Brenner and Rector's The Kidney, 8th ed.

CHAPTER 27. Diagnostic Kidney Imaging

William D. Boswell Jr.   Hossein Jadvar   Suzanne L. Palmer



Plain Film of the Abdomen, 839



Intravenous Urography, 839



Iodinated Contrast Media, 840



Ultrasound, 842



Ultrasound—Normal Anatomy, 842



Computed Tomography, 845



Computed Tomography Technique, 846



Computed Tomography Anatomy, 846



Magnetic Resonance Imaging, 846



Magnetic Resonance Imaging Protocols, 850



Diagnostic Magnetic Resonance Imaging; Routine Renal Exam, 850



Renal Vascular Evaluation; Magnetic Resonance Angiography/Venography, 852



Collecting System Evaluation: Magnetic Resonance Urography, 852



Nuclear Medicine, 853



Radiopharmaceuticals, 853



Normal Renal Function, 855



Kidney Injury—Acute and Chronic, 857



Unilateral Obstruction, 860



Renal Calcifications and Renal Stone Disease, 865



Renal Infection, 868



Renal Mass—Cysts to Renal Cell Carcinoma, 877



Renal Cancer—PET and PET-CT, 894



Renal Vascular Disease, 897



Nuclear Imaging and Renovascular Disease, 902



Renal Vein Thrombosis, 904



Renal Transplantation Assessment, 905

Imaging has evolved over the past 100 plus years, but the most changes have been seen in the past 20 years with marked changes in technology. In the beginning only anatomic information was available. Many different imaging examinations are now performed for the evaluation of the kidneys and the urinary tract provid-ing not only anatomic, but also functional and metabolic information. X-ray studies include plain films, intravenous urography (IVU), antegrade and retrograde pyelograms, and computed tomography (CT). Most of these studies provide anatomic information, as does ultrasound, which employs high-frequency sound waves, not ionizing radiation. Magnetic resonance imaging (MRI) yields primarily anatomic information, but shows potential for func-tional evaluation as well. Nuclear medicine studies contribute primarily functional information with positron emission tomography (PET) yielding a means of metabolic assessment. Each modality has something to offer in the evaluation of the kidney as technical advances in all the areas have led to better means for renal evaluation. To properly evaluate the clinical question in patients, it is important to understand the benefits, the limitations, and the diagnostic yields of each modality.


The plain film of the abdomen has been used for years as the starting point or first step in the evaluation of the kidneys as well as the rest of the abdomen. This study may also be known as the KUB or radiograph of the kidneys, ureters, and bladder ( Fig. 27-1 ). It is the scout film, first film, for many studies of the abdomen, including the IVU. The examination itself yields little significant information on its own. Renal size and contour may be estimated if the renal outlines can be seen, calcifications may be visualized, and other findings in the abdomen may be noted. If performed, it should be only the starting point in the evaluation of the kidneys. Intravenous iodinated contrast material is usually necessary for the opacification of the kidneys and urinary tract on radiograph examinations.



FIGURE 27-1  Plain film of the abdomen or KUB. The kidneys lie posteriorly in the retroperitoneum in the upper abdomen. They may be seen because they are surrounded by fat. The ribs overlie the kidney and bowel gas can be seen in the right upper quadrant. The psoas muscles are also well seen because retroperitoneal fat abuts them.




The intravenous urography (IVU) is still used by many as the primary means of investigation of the kidneys and urinary tract. [1] [2] The IVU is also known as the intravenous pyelogram (IVP). The manner in which it is performed is best tailored to the clinical problem that is being studied. A scout film or plain film of the abdomen (KUB) is done before any contrast material is injected intravenously. This provides a starting point for the investigation of the urinary tract, but also serves as an overall assessment of the abdomen and pelvis in general. Subsequently, 25 grams to 40 grams of iodine in the form of iodinated contrast media (generally 75 cc to 150 cc) are injected intravenously for the study. The method of choice is a bolus injection, which leads to peak iodine concentrations in the plasma. Infusion techniques for contrast media injection have been used in the past but lead to a lower peak iodine concentra-tion and poorer assessment overall. Timed sequential images of the kidneys and remainder of the genitourinary system are then obtained. [3] [4]

As the iodinated contrast media is filtered by the glomerulus, the plasma iodine concentration determines the concentration of iodine in the glomerular filtrate. The higher the concentration of iodine injected, the greater the amount of iodine within the kidney and thus the better visualization of the kidney and subsequently the pelvocalyceal system.[5] The first film obtained in an IVU is taken immediately after the completion of the injection of the contrast media (generally within 30 to 60 seconds). It will demonstrate a nephrogram or image of the kidneys that reflects the iodine concentration within the tubular system of the kidneys ( Fig. 27-2 ).[6] A higher plasma concen-tration of iodine leads to a higher iodine concentration in the glomerular filtrate. A higher iodine concentration in the tubular system results in a denser nephrogram or better depiction of the kidneys. This nephrogram may be used to evaluate the size, shape, and contour of the kidneys. The overall appearance and density of the kidneys should be symmetrical. The outlines of the kidneys are usually well seen contrasted by the lower or darker appearance of perirenal fat. The presence of renal cortical scars and contour abnormalities caused by renal masses are usually well seen. The kidneys are usually homogenous in appearance throughout with a cyst or mass within the kidney causing an alteration to the overall density of the kidney.



FIGURE 27-2  Intravenous urography—Nephrogram phase. This film is obtained within 60 seconds of the injection of contrast material. The kidneys are seen with smooth borders with the overlying bowel gas.



By 3 to 5 minutes after the completion of the injection of contrast material, the iodinated contrast has reached the calyceal system. The excretion of the contrast media by the kidneys should always be symmetrical and the time of appearance of contrast in the calyces similar. The anatomic depiction of the calyces, infundibula, and pelvis is best displayed by 5 to 10 minutes. Tomography may be performed, usually at 5 to 7 minutes, and it assists in the delineation of the renal contours, calyceal system, and renal pelvis ( Fig. 27-3 ). The calyces have a well-formed cup shape with sharp fornices and end in a thin smooth infundibulum, which leads into the renal pelvis. The calyces may be compound or complex with several ending in one infundibulum. Abdominal compression may improve visualization of the renal elements early in the study with subsequent release allowing for the drainage of the contrast into the ureters and better visualization of the ureters. Imaging of the ureters is usually accomplished at 10 to 15 minutes. The drainage of the contrast material from the kidney and ureters allows for a global assessment of the urinary bladder ( Fig. 27-4 ). The total number of images for the complete study is driven by the clinical question to be answered. [2] [3] [4]



FIGURE 27-3  Intravenous urography—Nephrotomogram. This film is obtained between 5 to 7 minutes after the injection of contrast material. The overall outline of kidney is well seen with the calyces, renal pelvis, and proximal ureter opacified with the excreted contrast.





FIGURE 27-4  Intravenous urography—Excretory phase. This film is obtained 10 minutes after the injection of the contrast material. The kidneys are well visualized with contrast outlining the calyces, pelvis, ureters, and bladder.




Over the years, many different intravascular contrast media have been employed.[7] All these contrast agents contain iodine in the form of a tri-iodinated benzoic acid ring in solution. Contrast agents are characterized as either ionic or nonionic and either monomers or dimmers. These agents are also known as high osmolar contrast media (HOCM), low osmolar contrast media (LOCM), and isotonic contrast media (IOCM) depending on their osmolality relative to plasma. HOCM has been used successfully for more than 50 years through the 1990's for most intravascular applications, including IVU, CT scanning, and angiographic applications. With the introduction of LOCM in the mid-1980's and IOCM in the 1990's, there has been a gradual shift to these agents. In the mid-2000's virtually all studies needing intravascular contrast injection are now performed with LOCM or IOCM.

All the HOCM agents are ionic. They are categorized as diatrizoates, iothalamates, and metrizoates. These compounds are all water-soluble salt solutions and all are hyperosmolar with relationship to plasma. The osmolality of these compounds is generally 5 to 8 times that of plasma (300 mOsm/liter). The anion is the iodine containing portion of the salt with the cation generally being either sodium or meglumine. Ionic media dissociate in water, whereas non-ionic media remains in solution. Within the bloodstream, these agents are not bound to any plasma proteins and therefore filtered by the glomerulus directly. Virtually all of the contrast media injected is filtered by the glomerulus with no tubular reabsorption of excretion in the patient with normal renal function.[7] For patients experiencing renal failure, contrast media may be excreted by other routes including the biliary system or GI tract. All iodinated contrast agents are dialyzable.

Contrast material within the plasma has a half-life of 1 to 2 hours in the patient with normal renal function. Virtually all contrast will be excreted by the kidneys within 24 hours. The volume of contrast material injected, the concentration of contrast within the plasma, and the glomerular filtration rate (GFR) determine the amount of contrast material excreted into the collecting systems and subsequently the calyces, renal pelvis, and ureters. Thus, in patients with normal renal function the concentration of iodine in the plasma will ultimately determine the quality of the study. Other factors, most particularly the state of hydration, also come into play as well. Changes in the tubular reabsorption of water along the nephron will affect the concentration of iodine within the tubule and thus the subsequent iodine concentration in the urine, which is visualized in the calyces and renal pelvis on the radiograph studies.

Most LOCM agents are nonionic compounds, with the exception of Ioxaglate, which is an ionic dimer.[8] These compounds do not dissociate in solution. The LOCM are still hyperosmolar relative to plasma but to a much lesser degree compared with HOCM. LOCM are generally 2 to 3 times the osmolality of plasma. These agents are filtered by the glomerulus, just as HOCM, but have a higher concentration within the tubular system because there is less water reabsorption. The osmotic affect of LOCM is less than HOCM in the tubular system and with a higher overall concentration; therefore, within the urine, the quality of imaging studies are generally improved.[9] Iohexol, Iopamidol, and Ioversol make up the group of nonionic LOCM.

Isotonic contrast media (IOCM) are nonionic dimers: Iodixanol and Iotrol. These agents are isotonic relative to plasma. They are handled in the kidney, just as HOCM and LOCM, filtered by the glomerulus with no tubular reabsorption or excretion. These agents are generally not used for renal imaging. Their use is almost exclusively for cardiac catherizations. Cost is the major difference with IOCM being 2 to 4 times higher.

Reactions to the injection of any of the contrast agents may occur. These reactions are not “allergic” in the sense of an antigen-antibody reaction.[10] No antibodies to contrast media have ever been isolated. The reactions, however, have the appearance of an allergic reaction. Although the majority of these reactions are mild or minor, severe reactions and deaths do occur. With ionic HOCM the reaction rate for the general population is 5% to 6%.[11] In patients with a history of allergy, the reaction rate is 10% to 12% and in those who have had a previous reaction to IV contrast administration the rate is 15% to 20%. The rate of reactions with LOCM and IOCM is much lower. [12] [13] Most reactions are mild consisting of flushing, nausea, and vomiting and do not require treatment. Mild dermal reactions, primarily urtica, do occur and may or may not require treatment. Moderate and severe reactions occur with considerably less frequency and include bronchospasm, laryngeal edema, seizures, arrhythmias, syncope shock, and cardiac arrest. All moderate and severe reactions require treatment. The risk of death has decreased from 1 in 8000 to 12,000 with HOCM and to 1 in 75,000 to 100,000 with LOCM and IOCM.[12]

As the reaction that occurs in patients after contrast injection is not antigen-antibody medicated, pretesting plays no role.[14] Neither the rate of injection nor dose of contrast material has been clearly established as a determinant in the occurrence of contrast-related reactions. [12] [15] Premedication with antihistamines is used in some patients with prior minor reactions. The use of glucocorticoids plus H1 & H2 blockers is reserved for patients who need to be studied with iodinated contrast agents and have a history of prior contrast related reaction—usually moderate or severe in nature. There are few if any controlled studies available to critically evaluate this pretreatment regime.[16]

Contrast-related nephropathy occurs with a significant frequency, especially in the hospitalized patient base. Acute kidney injury (AKI/ARF) resulting from the administration of iodinated contrast agents is the third leading cause of hospital acquired AKI/ARF, after surgery and hypotension. [17] [18] [19] The etiology of contrast-related nephropathy is unknown but felt to be multifactorial.[19] Contrast-induced nephropathy is commonly defined as acute kidney injury occurring within 48 hours of the administration of intravascular iodinated contrast material and that no other causes are readily apparent. The definition is actually quite variable within the literature, but is most commonly associated with a rise of 0.5 mg/dL of serum creatinine above a baseline value. [20] [21]

Most cases of contrast-related nephropathy present as an asymptomatic transient decrease in renal function and are nonoliguric. The rise in serum creatinine usually peaks at 3 to 5 days with a return to baseline within 10 to 14 days. Oliguric kidney injury occurs in a much smaller group with a peak creatinine elevation at 5 to 10 days and a return to baseline by 14 to 21 days. Rarely, oliguric kidney injury related to contrast media administration may require transient or long-term dialysis.

Risk factors for patients who may develop contrast-induced acute kidney injury are well known.[22] These include preexisting renal impairment, diabetes with renal insufficiency, dehydration, advancing age, congestive heart failure, ongoing treatment with nephrotoxic drugs, peripheral vascular disease, multiple myeloma, cirrhosis and liver failure, prior contrast load within 48 to 72 hours, and diuretic use, especially furosemide. [23] [24] Contrast-related AKI/ARF rarely if ever occurs in individuals who are well hydrated and have normal renal function. [25] [26] Although there is somewhat conflicting data, contrast-related nephropathy occurs with all types of contrast material. [20] [27] [28] Prevention of contrast-induced nephropathy is best done by recognizing the known risk factors.[29] Proper hydration is of paramount importance and must be performed beginning 12 hours before the contrast study. [30] [31]Various methods of pretreatment have been tried with variable success. These include mannitol, diuretics, calcium channel blockers, adenosine antagonists (Theophylline), dopamine agonists, N-acetylcysteine, and sodium bicarbonate. [32] [33] [34] [35] Again, with appropriate hydration and normal renal function, contrast-related nephropathy rarely occurs.


Ultrasonography is a leading diagnostic examination used in the investigation of the kidneys and urinary tract.[36] It is noninvasive and requires little or no patient preparation. It is the first-line examination in the azotemic patient for assessing renal size and the presence or absence of hydronephrosis and obstruction. It is used to assess the vasculature of native and transplanted kidneys. Renal morphology and the characterization of renal masses are also done with ultrasound. As a guide for renal biopsy, ultrasound has helped to decrease morbidity and mortality.

Diagnostic ultrasonography is an outgrowth of SONAR (Sound Navigation and Ranging technology) used first during World War II for the detection of objects underwater. Medical ultrasound uses high-frequency sound waves to investigate diagnostic problems. In the abdomen and more particularly the kidney, 2.5 mHz to 4.0 mHz sound waves are generally employed.

The ultrasound unit consists of a transducer that sends and receives the sound waves, a microprocessor or computer that acquires and processes the returning signal, and an image display system or monitor that displays the processed images. The piezoelectric transducer converts electrical energy into high-frequency sound waves that are transmitted through the patient. It converts the returning reflected sound waves back into electrical energy that can be processed by the computer. Sound travels as a waveform through the tissues being imaged. The speed of the sound wave depends on the tissue through which it is traveling. In air, sound travels at 331 M/second and in the soft tissues of the body it travels at approximately 1540 M/second.

Different tissues and the interface between these tissues have different acoustic impedance. As the sound wave travels through different tissues, part of the wave is reflected back to the transducer. The depth of the tissue interface is measured by the time the sound wave takes to return to the transducer. A grey-scale image is produced by the measured reflected sound with the intensity of the pixels (picture elements) being proportional to the intensities of the reflected sound ( Fig. 27-5 ). When the acoustic interfaces are quite large, strong echoes result. These are known as specular reflectors are a seen from the renal capsule and bladder wall. Non-specular reflectors generate lower amplitude echoes are seen in the renal parenchyma. Strong reflection of sound by bone and air results in little or no information from the tissues beneath; this is known as shadowing. Lack of acoustic impedance as seen in fluid-filled structures, such as the urinary bladder and renal cysts, allows the sound waves to penetrate further resulting in a relative increase in intensity distal to the structures; this is known as increased through transmission. Real-time ultrasound, which provides sequential images at a rapid frame rate, allows the demonstration of motion of organs and pulsation of vessels.



FIGURE 27-5  Normal renal ultrasounds. Normal right kidneys (A, C) and left kidneys (B, D) are shown. The central echogenic structure represents the vascular elements, calyces, and renal sinus fat. The peripheral cortex is noted to be smooth and regular. Renal pyramids are seen as hypoechoic structures between the central echo complex and the cortex in D.



Doppler ultrasound, based on the Doppler frequency shift of the sound wave caused by moving objects, can be used to assess venous and arterial blood flow ( Fig. 27-6 ). [37] [38] Assessment of the waveforms can be used in diagnosis. The peripheral arterial resistance can be measured within the kidney. (Resistive Index RI = Peak Systolic velocity - lowest Diastolic velocity/Peak systolic velocity) ( Fig. 27-7 ). Generally speaking, a normal RI is 0.70 or less. Native and transplanted kidneys can be evaluated. Increased RI is a nonspecific indicator of disease and a sign of increased peripheral vascular resistance.[39] With color Doppler ultrasound, the image is encoded with colors assigned to the pixels representing the direction, velocity, and volume of flow within vessels.[38] Power Doppler ultrasound uses the amplitude of the signal to produce a color map of the intrarenal vasculature and flow within the kidney ( Fig. 27-8 ).[37]



FIGURE 27-6  Normal color Doppler ultrasound. Normal right (A) and left (B) kidneys are seen. The red echogenic areas represent arterial flow (flow toward the transducer) and blue echogenic areas venous flow (flow away from the transducer).





FIGURE 27-7  Normal power Doppler ultrasound. Normal right (A) and left (B) kidneys are seen. The color image represents a summation of all flow—arterial and venous—within the kidney.





FIGURE 27-8  Normal duplex Doppler ultrasound. Normal right (A) and left (B) kidneys are seen. The waveforms within the interlobar arteries are visualized with the resistive indices calculated for each kidney.



Ultrasound—Normal Anatomy

The kidneys are located within Gerota's fascia and are surrounded by perinephric fat in the retropertoneum. Sonographic images of the kidneys are generally obtained in the longitudinal and transverse planes. Parasagittal images are also obtained.[40] The perinephric fat has a variable appearance from slightly less echogenic to highly echogenic compared with the renal cortex. The renal capsule is seen as an echogenic line surrounding the kidney. The centrally located renal sinus or hilum, containing renal sinus fat, vessels, and the collecting system, is usually echogenic due to the presence of renal sinus fat (see Fig. 27-5 ). The amount of renal sinus fat generally increases with age. Tubular structures may be seen in the renal hilum corresponding to vessels and the collecting system. Color Doppler ultrasound may be used to differentiate the vessels from the collecting system.

Overall renal echogenicity is generally compared with the liver on the right and the spleen on the left (see Fig. 27-5 ). The normal renal cortex is less echogenic than the liver and spleen. Underlying liver disease may alter this picture. The medullary pyramids are hypoechoic and their triangular shape points to the renal hilum. The renal cortex lies peripherally and the separation from the medulla is usually demarcated by an echogenic focus due to the arcuate arteries along the corticomedullary junction. Columns of Bertin have the same echogenicity as the renal cortex and separate the renal pyramids. Occasionally a large column of Bertin may be seen and simulate a mass, a “pseudotumor.” Even when large or prominent, a column of Bertin maintains similar echogenicity to the cortex and the vascular pattern seen on power Doppler image is also the same.

Renal size is easily measured sonographically. The normal longitudinal dimension of right kidney is 11 cm ± 1 cm and the left kidney is 11.5 cm ± 1 cm. The contours of the kidney are usually smooth although there may occasionally be some slight nodularity due to fetal lobulation. The renal arteries and veins may be seen extending from the renal hilum to the aorta and inferior vena cava. The veins lie anterior to the arteries. The renal arterial branching pattern within the kidneys may be seen with color Doppler sonography (see Fig. 27-6 ).[41] The resistive indices (RI) of the main, intralobar, and arcuate vessels may be calculated (see Fig. 27-7 ). With power Doppler imaging the intrarenal vasculature may be assessed demonstrating an overall increased pattern in the cortex relative to the medulla, corresponding to the normal arterial flow to the kidney (see Fig. 27-8 ). [42] [43] The renal calyces and collecting systems are not typically seen with ultrasound unless there is fullness or distension caused by a diuresis or obstruction. When seen the collecting systems are branching anechoic structures in the renal sinus fat connecting together to the renal pelvis. The urinary bladder is seen in the pelvis as a fluid-filled sonolucent structure. The entrance of the ureters into the bladder at the trigone may be visualized using color Doppler sonography. Ureteral jets should be seen bilaterally.

When a kidney is not identified in its normal location in the retroperitoneum, assessment of the remainder of the abdomen and pelvis should be undertaken. Ectopic kidneys may lie lower in the abdomen or within the pelvis and may also be located on the opposite side, even fused with the other kidney. Horseshoe kidneys tend to lie lower in the retropertoneum and the axes of the kidneys may be different than the normal kidney.

The demonstration of increased echogenicity within the renal cortex may be useful in suggesting the presence of renal parenchymal (medical renal) disease. [43] [44] The renal cortex may show increased echogenicity in patients with either acute or chronic kidney injury. This finding is nonspecific and does not correlate with the degree or severity of kidney injury. The finding is bilateral. The increased cortical echogenicity in patients with chronic kidney injury is generally related to interstitial fibrosis.[39] A patient with small, echogenic kidneys usually has end-stage renal disease (ESRD). Ultrasound has been very useful in directing renal biopsy for patients with either acute or chronic kidney injury. Renal identification and localization greatly facilitates the procedure. Its use has decreased the procedure time as well as decreased morbidity and mortality.


Computed tomography (CT) has become an essential tool for diagnosis in virtually all areas of the body. In the genitourinary tract, it has supplanted the IVU, which had been the mainstay of diagnosis for years. Even in areas where ultrasound is employed, CT offers a complementary and sometimes superior means of imaging. CT is now the first examination to be performed in patients with renal colic, renal stone disease, renal trauma, renal infection and abscess, renal mass, hematuria, and finally, urothelial abnormalities.

Computed tomography has been heralded as the greatest improvement in diagnostic radiology since Roentgen discovered x-rays in 1895. Sir Godfrey Hounsfield developed the first CT scanner in 1970.[45] The first clinical applications in 1971 were in the head. The first body CT scanner was installed in Georgetown University Medical Center in 1974. The field has grown rapidly since that time with new technical innovations, image processing, and visualization methods. For his outstanding work in the field and for demonstrating the unique and remarkable clinical capabilities of CT, Sir Godfrey Hounsfield was awarded the Nobel Prize for Medicine in 1979.

Computer tomography is the computer reconstruction of an x-ray-generated image that typically depicts a slice through the area being studied in the body. The x-ray tube produces a highly collimated fan-bean and is mounted opposite an array of electronic detectors. This system rotates in tandem around the patient. The detector system collects hundreds of thousands of samples representing the x-ray attenuation along the line formed from the x-ray source to the detector as the rotation occurs. These data are transferred to a computer, which reconstructs the image. The image may then be displayed on a computer monitor or transferred to radiograph film for reviewing.

The CT image is actually made up of numerous pixels (picture elements) each corresponding to a CT number representing the amount of x-rays absorbed by the patient at a particular point in the cross-sectional image. These pixels represent a 2D display of a 3D object. Each pixel element actually has a third dimension—the slice thickness or depth. Thus, the CT number is actually the average x-ray attenuation of all the tissues within a specific volume element, voxel, which is used to create the individual image or slice.

Computed tomography numbers are the x-ray attenuation of each voxel relative to the attenuation of water (CT number = 0). Tissues that attenuate more x-rays than water have positive CT numbers and those with less attenuation have negative numbers. Bone may have a CT number greater than 1000, with air in the lungs having a CT number of ≈ -1000. Different shades of grey on a scale of white to black are assigned to the CT numbers (highest = white, lowest = black). The image of each slice is thus created on the monitor with image manipulation possible to accentuate the regions being imaged. The image data is constant but by varying the range of CT numbers, the appearance of the image may be changed, a key element of any digital image.

The initial CT scanners were relatively slow as the technology required a point and shoot process. One slice was obtained, the patient moved, and the next slice obtained. This initial generation of body CT scanner led to a scan of the abdomen that took up to 2 to 4 minutes or more to complete. In 1990, helical/spiral technology was introduced in which the x-ray tube and detector system continuously rotated around the patient and the patient moved continuously through the gantry. Scan time was reduced to 25 to 35 seconds through the abdomen. After helical/spiral CT, a two detector system was introduced that produced two slices for every 360° rotation of the x-ray tube and detector system. This was the first multi-detector CT scanner (MDCT). By 1998, four-detector systems were introduced by all manufactures. Today 10, 16, 32, 40, and 64 detector systems are available with more technological advances on the horizon. With MDCT, each 360° rotation of results in the number of slices equal to the number of detectors (i.e., 64 detector system = 64 slices in one 360° rotation). These technological advances have led to dramatic increase in the speed of scans (4 to 10 seconds), routine use of thin slices or collimation (1 mm to 2 mm), and marked improvement in spatial resolution (ability to resolve small objects).[46]

The faster scan times have led to improved utilization and optimization of intravenous contract enhancement.[47] For example, the kidney can be scanned in the arterial, venous, nephrographic, and delay phases allowing for a more complete assessment. With a 16-64 detector scan, a single acquisition of CT data takes from 3 to 7 seconds with slice thickness being less than 1 mm. The images are normally displayed as transverse or axial images. As the slice thickness has been reduced to the point that the voxel has become a cube or near cube (isotropic voxel), sagittal, coronal, and oblique image may be displayed with no loss of resolution. The data acquisition may also be displayed as a 3D volumetric display with the regions of interest highlighted.[47] Scanning today is done with a single breath hold acquisitions leading to the elimination of virtually all motion artifacts, and the misregistration artifacts seen with breathing. In imaging the heart, ECG gated-acquisition to the cardiac cycle eliminates the motion of the heart resulting in clear assessment of the coronary arteries, valves, and related anatomy. The kidney is well suited for assessment with MDCT as sagittal, coronal, and 3D displays are additive to the information content of the study. [47] [48] [49] [50] [51]

Computed tomography urogram was introduced in 1999 to 2000 and is an outgrowth of the advances made with MDCT technology and state-of-the-art workstations with their added computer processing and display capabilities. [46] [52] The CT urogram provides a complete examination of the kidney and the remainder of genitourinary tract. CT urography assesses the kidney as a whole (anatomic), the vascular tree (function and perfusion), and the excretory (urothelial) patterns. Noncontrast scans provide for assessment of renal calculi, high density cysts, and contour abnormalities.[53] Early phase scans (12–15 seconds) leads to arterial assessment. Scanning at 25 to 30 seconds yields a combined arterial-venous phase image with clear corticomedullary differentiation. With imaging done at 90 to 100 seconds, true nephrographic phase imaging of the kidneys is obtained.[47] Delayed imaging, typically at 3 to 7 minutes and up to 10 minutes, provides excretory phase images with evaluation of the urothelium—calyces, renal pelvis, ureters, and bladder.[54] Axial images, multiplanar reconstructions, maximum intensity projection (MIP) images, and 3D volumetric displays complement each other in the CT urogram.[52] Properly performed, the CT urogram has replaced the IVU in 2005. [55] [56] [57] [58]

Computed Tomography Technique

Noncontrast images are obtained through the kidneys and the remainder of the GU tract to the pelvic floor if stone disease is the primary problem. In the case of vascular problems and renal masses, arterial-venous phase imaging is usually required and accomplished by a rapid bolus injection of iodinated contrast media, generally 4 to 5 cc/second and a volume of 100 to 120 cc, with scans in the arterial-venous phases at 25 to 30 seconds. When needed as in cases of suspected renal artery stenosis, true arterial phase imaging may be performed beginning at 12 to 15 seconds. Nephrographic imaging at 90 to 100 seconds is subsequently performed with excretory imaging to follow. Slice thickness is general 2 mm or less, which will allow for workstation reconstruction as necessary. The radiation dose for this technique is approximately 1.5 times that of the IVU, but the information content is exceedingly higher.

Computed Tomography Anatomy

The kidneys lie in the retroperitoneum, surrounded by Gerota's fascia in the perinephric space. Fat will generally outline the kidneys with the liver anterior-superior on the right, the spleen superior on the left, and the spine, aorta, and inferior vena cava (IVC) central to each kidney ( Fig. 27-9 ). The abdominal contents lie anteriorly. This anatomy is easily seen with all phases of scanning. With arterial and venous phase scans, the renal arteries are easily seen, generally posterior to the venous structures ( Fig. 27-10 ). The right renal artery is located behind the IVC ( Fig. 27-11 ). The left renal vein courses anterior to the aorta before it enters the IVC and the right renal vein generally is seen obliquely entering the IVC. The adrenal glands are found in a location superior to the upper poles of the kidneys. In venous phase imaging, true separation of the renal cortex from the medulla is easily accomplished. Cortical thickness and medullary appearance may easily be assessed (see Fig. 27-10 ). The nephrographic phase should demonstrate the symmetrical enhancement for each of the kidneys ( Fig. 27-12 ).[47] At 7 to 10 minutes in the excretory phase, the calyces should be well seen with sharp fornices, a cupped central section, and a narrow smooth infundibulum leading to the renal pelvis ( Fig. 27-13 ).[54] Coronal images in a slab MIP format will display this to the best advantage. Three-dimensional volumetric reformations also may display the anatomic delay ( Fig. 27-14 ).[57] The excretory phase images also delineate the ureters from the renal pelvis to the bladder. A curved reformatted series of images or 3D display will be needed to display the ureters in their entirety. Proper tailoring of the examination to the diagnostic problem will lead the correct imaging acquisition. [48] [50] [58]



FIGURE 27-9  Normal noncontrast CT scan through the mid-portion of the kidneys. The kidneys lie in the retroperitoneum with the lumbar spine and psaos muscles more centrally. The liver is seen anterolateral to the right kidney and the spleen anterolateral to the left kidney.





FIGURE 27-10  Normal corticomedullary phase CT scan. Axial CT slice (A) and coronal image (B) demonstrate the dense enhancement of the cortex relative to the medulla containing the renal pyramids.





FIGURE 27-11  Normal renal CT angiogram. The aorta and the exiting renal arteries on the right and left are seen. The kidneys are seen peripherally with the branching renal arteries.





FIGURE 27-12  Normal nephrogram phase CT scan. The axial image (A) and the coronal image (B) demonstrate the homogenous appearance of the kidneys with the cortex and medulla no longer differentially enhanced. These images are typically obtained at 80 to 120 seconds after the injection of contrast material.





FIGURE 27-13  Normal excretory phase CT scan. The calyces and renal pelvis are now easily noted as they are opacified by the excreted contrast. This scan is obtained 5 to 10 minutes after the injection of contrast material.





FIGURE 27-14  Normal CT urogram. The maximum-intensity projection (MIP) image (A) and volume rendered image (B) demonstrate the calyces, renal pelvis, ureters, and bladder. The MIP image is a slab—15 mm thick done in the coronal plane. The volume rendered image as the extraneous tissues adjacent to the kidneys removed and highlight the genitourinary track.




Like CT, magnetic resonance imaging (MRI) is a computer-based, multiplanar imaging modality. But instead of using ionizing radiation, MRI uses electromagnetic radiation. MRI is an alternative to contrast-enhanced CT, especially in patients with iodinated contrast allergy and renal insufficiency. MRI is also used when reduction of radiation exposure is desired, such as during pregnancy and in the pediatric population. MRI routinely allows detailed tissue characterization of the kidney and surrounding structures. The physics behind MRI is complex and will only be addressed briefly.

Clinical MRI is based on the interaction of hydrogen ions (protons) and radiofrequency waves in the presence of a strong magnetic field. [59] [60] [61] The strong magnetic field, called the external magnetic field, is generated by a large bore, high field strength magnet. Most magnets in clinical use are superconducting magnets. The magnet strength is measured in Tesla (T) and can range from 0.2T to 3T for clinical imaging and up to 15T for animal research. Renal imaging is performed best on high field magnets (1.5T–3T) that allow for higher spatial resolution and faster imaging.

Images of the patient are obtained through a multistep process of energy transfer and signal transmission. When a patient is placed in the magnet, the mobile protons associated with fat and water molecules align longitudinal to the external magnetic field. No signal is obtained unless a resonant radiofrequency (RF) pulse is applied to the patient. The RF pulse causes the mobile protons within the patient to move from a lower, stable energy state to a higher, unstable energy state (excitation). When the RF pulse is removed, the protons return to the lower energy steady state while emitting frequency transmissions or signals (relaxation). In radiology lingo, an external RF pulse “excites” the protons causing them to “flip” to a higher energy state. When the RF pulse is removed, the protons “relax” with emission of a “radio signal”. The signals produced during proton relaxation are separated from one another with applied magnetic field gradients. The emitted signals are captured by a receiving coil and reconstructed into images through a complex computerized algorithm: the Fourier Transform. [59] [60] [61]

Different tissues have different relaxation rates that lead to different levels of signal production or signal intensity. The signal intensity of each tissue is determined by three characteristics:



Proton density of the tissue. The greater the number of mobile protons, the greater the signal produced by the tissue. For example: a volume of urine has more mobile protons than the same volume of renal tissue, therefore urine will give more signal than the kidney. Stones have far fewer mobile protons per unit volume and therefore will produce little signal.



T1 relaxation time. How quickly a proton returns to the pre-excitation energy state. The shortest T1 times (rapid relaxation) produce the strongest signal.



T2 relaxation time. How quickly the proton signal decays due to non-uniformity of the magnetic field. A non-uniform field accelerates signal decay and leads to signal loss. [59] [60] [61]

Magnetic resonance imaging involves the acquisition of multiple pulse sequences. A pulse sequence is a set of defined RF pulses and timing parameters used to acquire image data. These sequences include, but are not limited to, spin echo, gradient echo, inversion recovery, and steady-state precession. The data are acquired in volumes (voxels), reconstructed as 2D pixels, and displayed relative to tissue signal intensity variations (tissue contrast). Tissue contrast, like signal intensity, is determined by proton density and relaxation times. T1 weighting is related to the rate of T1 relaxation and the pulse repetition time (TR), also known as the time allowed for relaxation. T2 weighting is related to the rate of T2 relaxation and the time at which the “radio signal” is sampled by the receiver coil, also known as the time to echo (TE). TR and TE are programmable parameters that can be altered to accentuate T1 and T2 contrast weighting. [59] [60] [61] For the general observer, T1-weighted sequences have short TR and TE and show simple fluid as black. T2-weighted sequences have long TR and TE and show simple fluid as white ( Fig. 27-15 ).



FIGURE 27-15  Normal MR signal characteristics of simple fluids. A, Urine is dark on T1-weighted sequences and (B) bright on T2-weighted sequences.



There are many programmable parameters, other than TR and TE, used to optimize imaging. These include, but are not limited to, choice of pulse sequence, coil types and gradients, slice orientation and thickness, field of view and matrix, gating to reduce motion, and use of intravenous (IV) contrast. Although there are many pulse sequences used in clinical MR imaging, ultrafast sequences are preferred for renal imaging. These fast sequences can be acquired in less than 30 seconds while the patients hold their breath. The benefits of rapid acquisition include improved image quality due to reduction of motion artifact, reduction of total scan time, and the ability to perform dynamic imaging.[62]

Use of IV contrast is routine in renal imaging due to the improved lesion detection and diagnostic accuracy provided by IV gadolinium-chelates (Gd-C). Gadolinium is a paramagnetic substance that shortens the T1 and T2 relaxation times, resulting in increased signal intensity on T1-weighted images and decreased signal intensity on T2-weighted sequences ( Fig. 27-16 ). The pharmacokinetics and enhancement patterns of IV Gd-C agents are similar to iodinated contrast agents used for radiograph examinations. Unlike iodinated contrast agents, the dose response to Gd-C is non-linear; the signal intensity increases at low concentrations and then decreases at higher concentrations. Hence, the collecting systems, ureters, and bladder first brighten and then darken on T1-weighted sequences as the gadolinium concentration within the urine increases. Gd-C agents are well tolerated and can be used in patients with iodinated contrast allergies or who have renal insufficiency.[63] Severe contrast reactions to Gd-C agents are rare, as is nephrotoxicity. [64] [65] [66] There have been some reports of nephrotoxicity with IV Gd-C in high-risk populations: those with moderate to severe kidney injury. [67] [68] Gd-C may interfere with serum calcium and magnesium measurements, especially in patients with renal insufficiency.[69] As with iodinated contrast, dialysis filters Gd-C effectively and dialysis is therefore recommended after contrast use in patients with kidney injury.[70]



FIGURE 27-16  Paramagnetic effects of gadolinium on urine. A, Coronal T1-weighted image from an MR urogram demonstrates enhancement of the urine in the collection system. B, Coronal T2-weighted image from an MR urogram demonstrates low signal intensity urine in the collecting system secondary to effects of gadolinium. C, Axial T1-weighted, delayed post contrast image demonstrates layering of contrast. The denser, more concentrated gadolinium is dark (arrow). The less concentrated gadolinium is brighter and layers above (arrowhead).



Gd-C agents are not without risk, however. There have been recent reports of Gd-C associated development of nephrogenic systemic fibrosis (NSF), a rare fibrosing disease seen predominantly in dialysis dependent patients. [71] [72] [73] [74] [75] [76] NSF was first described in 1997 and published in the literature in 2000[77]; but it was not until January 2006 that a possible causal relationship between Gd-C and NSF was presented in the literature. To date, over 215 cases have been reported to the International Center for Nephrogenic Fibrosing Dermopathy (ICNFD).[78] A cause and effect link between Gd-C and NSF has not been proven as of yet, but NSF has been strongly associated with high dose IV gadodiamide administration in the setting of high-risk patients. Gadodiamide is one of 5 U.S. Food and Drug Administration (FDA) approved Gd-C contrast agents for MRI. High-risk patients include patients with dialysis dependent chronic renal insufficiency, low glomerular filtration rate (GFR) of <30 mL/min/1.73 m2 and acute hepatorenal syndrome. To date, no cases of NSF have been documented in patients with normal renal function.

Potential for NSF to occur in association with all the FDA approved Gd-C agents is suspected, but not proven. As more medical research is available, recommendations for the usage of Gd-C in patients with moderate to severe renal disease will be modified. [76] [79] At the time of publication of this book, our approach to the use of Gd-C in high-risk patients is as follows: We do not administer gadodiamide to our patients. The Gd chelates that we use are at the FDA approved doses, or lower. If the patient is high-risk (dialysis dependent chronic renal insufficiency, GFR of <30 mL/min/1.73 m2 or acute hepatorenal syndrome) we restrict the use of Gd-C agents to those patients who require contrast to make a diagnosis or direct therapy. We also recommend dialysis after exposure to Gd-C for dialysis dependent patients, although this has not been found to reduce the incidence of NSF. Suspected cases of NSF should be confirmed by skin biopsy and reported to ICNFD to help further our understanding of NSF and its association with Gd-C.

Contrast-enhanced MRI (CE-MRI) allows for dynamic evaluation of the kidney and surrounding structures. Serial acquisitions are obtained after bolus injection of gadolinium (0.1 mmol/kg–0.2 mmol/kg body weight) at 2 cc sec.[80] [81] The injection should be administered by means of an automatic, MR-compatible power injector to assure accuracy of the timed bolus, including volume and rate of injection. [81] [82] The corticomedullary/arterial phase (approximately 20 sec) best evaluates the arterial structures and corticomedullary differentiation. The nephrographic phase (70 to 90 sec) maximizes tumor detection and best demonstrates the renal veins and surrounding structures (Fig. 27-17 ). Imaging can be performed in any plane, but the coronal plane is the most frequently used for dynamic imaging as it allows imaging of the kidneys, ureters, vessels, and surrounding structures in the fewest number of images.



FIGURE 27-17  Magnetic resonance appearance of a normal kidney after bolus injection of gadolinium contrast material at (A) 20 seconds, (B) 50 seconds, and (C) 80 seconds after start of injection.



Magnetic resonance imaging is not indicated for every patient due to the presence of some implanted medical devices such as pacemakers, ferromagnetic CNS aneurysm clips, and ferromagnetic stapedial implants. Not all implants or devices are a problem, but knowledge of the type of device is critical to determine if the patient can safely enter the magnet.[83]


Diagnostic Magnetic Resonance Imaging; Routine Renal Exam

Routine MRI evaluation of the kidneys includes axial and coronal T1-weighted and T2-weighted sequences. Both can be obtained with and without fat suppression. Dynamic contrast-enhanced T1-weighted sequences are also routinely obtained. In patients with normal renal function the renal cortex and medullary pyramids are easily differentiated due to the excellent tissue differentiation provided by MRI. On T1-weighted sequences the renal cortex is higher in signal intensity than the medullary pyramids. On T2-weighted sequences the renal cortex is lower in signal intensity than the medullary pyramids ( Fig. 27-18 ). With kidney injury this corticomedullary differentiation disappears ( Fig. 27-19 ). [84] [85] Urine, like water, is normally black on T1-weighted and white on T2-weighted sequences (see Fig. 27-15 ). The parenchymal enhancement characteristics are similar to those seen on contrast-enhanced CT.



FIGURE 27-18  Normal MRI appearance of corticomedullary differentiation. A, Axial T1-weighted image demonstrates increased signal intensity of the renal cortex relative to the medullary pyramids. B, Axial T2-weighted image demonstrates decreased signal intensity of the renal cortex relative to the medullary pyramids.





FIGURE 27-19  Axial T2-weighted image demonstrates loss of corticomedullary differentiation in patient with elevated creatinine.



Renal Vascular Evaluation; Magnetic Resonance Angiography/Venography

On routine, precontrast imaging, the vessels can be variable in signal intensity, ranging from white to black due to many factors including, but not limited to, flow-related parameters, location and orientation of the imaged vessel, and choice of pulse sequence. Non contrast-enhanced pulse sequences can be used for angiography and venography, but these sequences take longer to acquire and their use is limited in abdominal imaging. These sequences are sometimes called “bright-blood” sequences and include time-of-flight MR angiography, which is based on flow-related enhancement, and phase contrast MR angiography, which is based on velocity and direction of flow. Phase contrast MR angiography can be used in conjunction with contrast-enhanced MR angiography (CE-MRA) to detect turbulent flow and high velocities associated with stenoses.

Unlike the “bright blood” sequences, CE-MRA minimizes flow-related enhancement and motion. CE-MRA depends on the T1 shortening properties of gadolinium, which allow for faster imaging, increased coverage, and improved resolution. [60] [86] Accurate timing of the contrast bolus is critical for CE-MRA. The time at which the bolus arrives at the renal arteries may be determined with a bolus injection of 1 cc of gadolinium followed by a saline flush. A 3D T1-weighted gradient-echo MR imaging pulse sequence is then acquired in the coronal plane during the injection of approximately 15 cc to 20 cc of gadolinium at 2 cc/sec, timed to capture the arterial phase. [80] [81] Sequential 3D sequences are acquired to capture the venous phase (MR venography). The data sets can be post processed into multiple formats, improving ease and accuracy of interpretation ( Fig. 27-20 ). [87] [88] [89]



FIGURE 27-20  Magnetic resonance angiogram reconstructed with 3D software. A, Demonstrates excellent visualization of small accessory right renal artery (arrow). B, Presents the accessory artery in a way to make more accurate luminal measurements.



Collecting System Evaluation: Magnetic Resonance Urography

Magnetic resonance urography (MRU) consists of protocols tailored to the evaluation of the renal collecting system and the pathology found there. MRU can be performed with heavily T2-weighted sequences, where urine gives the intrinsic contrast, or with contrast-enhanced T1-weighted sequences, which mimic conventional IV urography (IVU) and CT urography (CTU). Heavily T2-weighted sequences are most useful in patients with dilated collecting systems, where all water-filled structures are bright ( Fig. 27-21 ), and in patients with impaired renal excretion, where contrast urography is most limited. Unfortunately, without adequate distention of the collecting system, T2-weighted evaluation is limited. Although a good morphologic examination, T2-weighted urography is ultimately limited by a lack of functional information. For example, T2-weighted urography cannot reliably differentiate between an obstructed system and an ectatic collecting system ( Fig. 27-22 ).[90] Contrast-enhanced, excretory T1-weighted urography is superior to T2-weighted urography because both morphology and function can be evaluated. [90] [91] [92]



FIGURE 27-21  Bilateral hydronephrosis secondary to bladder tumor. A and B, Heavily T2W MRU demonstrate bilateral hydronephrosis and hydroureter due to bladder mass (arrow). C, Contrast-enhanced MRU nephrographic phase demonstrates asymmetric enhancement of the kidneys and (D) excretory phase demonstrates asymmetric excretion of gadolinium. There is no excretion on the right as demonstrated by unenhanced (dark) urine within the collecting system.





FIGURE 27-22  A and B, Coronal T2-weighed images demonstrate right renal atrophy and dilatation of the right collecting system in a patient after bladder resection and ilio-conduit reconstruction (arrow). On these static images it is difficult to differentiate between an obstructed and non obstructed system. This patient has pelvocaliectasis without obstruction, demonstrated on the contrast-enhanced portion of the examination.



T2- and contrast-enhanced T1-weighted sequences are complementary and are frequently acquired together as part of a complete MRU examination. In non dilated systems, both techniques require hydration and furosemide for adequate distention of the renal collecting system. [90] [93] A typical MRU will start with a coronal, heavily T2-weighted sequence where simple fluid (urine, CSF, ascites) is bright and all other tissues are dark (see Fig. 27-21 ). This rapid breath-hold sequence takes less than 5 seconds to acquire and is presented as a urographic-like image. The T2-weighted sequence is used as an initial survey of fluid within collecting system. Low-dose furosemide (0.1 mg/kg body weight, maximum dose 10 mg) is administered intravenously, 30 to 60 seconds before the intravenous administration of gadolinium (0.1 mmol/kg). [91] [92] Furosemide is given to increase urine volume and dilute the gadolinium within the collecting system. [91] [93] Coronal, post contrast, 3D T1-weighted sequences are acquired with the same technique as renal MRA, in the corticomedullary/arterial phase, nephrographic phase, and excretory phase (see Fig. 27-21 ).[92] Additional sequences may be acquired in any plane to better evaluate suspected pathology.

By combining renal MRI and MRU, a comprehensive morphologic and functional evaluation of urinary tract can be obtained. MRU gives accurate evaluation of the upper urinary tract, and is useful in the evaluation of anatomic anomalies including duplications, ureteropelvic obstruction, anomalous crossing vessels, and ureteroceles [93] [94] ( Fig. 27-23 ). Obstructive disease is well evaluated no matter whether the etiology is intrinsic or extrinsic to the collecting system.



FIGURE 27-23  Duplicated collecting system. A and B, Contrast-enhanced MRU demonstrates a duplicated collecting system on the right with delayed excretion of the upper pole moiety. C, Obstruction of the upper pole moiety is confirmed on intravenous urogram.




Scintigraphy offers imaging-based diagnostic information on renal structure and function. Many single-photon radiotracers have long been in routine clinical use in renal scintigraphy, which are tailored to provide physiological information complementing the primarily anatomic and structural-based imaging modalities such as ultrasonography (US), computed tomography (CT), and magnetic resonance imaging (MRI). With the rapid expansion of positron emission tomography, and more recently hybrid structural-functional imaging systems such as PET-CT, additional unprecedented opportunities have developed for quantitative imaging evaluation of renal diseases in clinical medicine and in the research arena. In this section, we review the unique contribution of scintigraphy, including PET, in the imaging evaluation of renal structure and function. We first launch with a brief discussion of the common radiopharmaceuticals used in renal scintigraphy.


Technetium 99m diethylenetriaminepentaacetic Acid (Tc-99m DTPA)

Tc-99m DTPA is the common agent for assessing glomerular filtration rate (GFR). The ideal agent for measuring GFR is cleared only by glomerular filtration and is not secreted or reabsorbed. Tc-99m DTPA satisfies the first requirement but has variable degrees of protein binding, which deviates its kinetics from the ideal agent such as inulin. For a 20 mCi (740 MBq) dose, the radiation exposures to the kidneys and to the urinary bladder are 1.8 rads and 2.3 rads, respectively.[95]

Iodine-131 Orthoiodohippurate (I-131 OIH)

The mechanism of I-131 OIH renal clearance is about 20% by GFR and about 80% by tubular secretion. I-131 OIH is an acceptable alternative to para-aminohippuric acid (PAH) for determining renal plasma flow although its clearance is 15% lower than that of PAH. PAH is not entirely cleared by the kidneys with about 10% of arterial PAH remaining in the renal venous blood. Therefore, I-131 OIH measures effective renal plasma flow (ERPF). The tubular extraction efficiency of I-131 OIH is 90% and there is no hepatobiliary excretion. OIH may also be labeled with I-123 that not only provides equivalent urinary kinetics as that for I-131 label but also offers improved image quality due to typically larger administered dose in view of its more favorable radiation exposure. For a 300 uCi (11 MBq) dose of I-131 OIH, the radiation exposures to the kidneys and to the urinary bladder are 0.02 rads and 1.4 rads, respectively. Few drops of nonradioactive iodine (e.g., saturated solution of potassium iodide) orally minimize the thyroid uptake of free I-131.[95]

Technetium 99m Mercaptoacetyltriglycine (Tc-99m MAG3)

Tc-99m MAG3 has similar properties to OIH but has significant advantages of better image quality and less radiation exposure. The tubular extraction fraction of MAG3 is lower than OIH at about 60% to 70%. There is also about 3% hepatobiliary excretion, which increases with renal insufficiency. Despite these features, however, MAG3 is a common agent used in scintigraphic evaluation of renal function. For a 10 mCi (370 MBq) dose, the radiation exposures to the kidneys and to the urinary bladder are 0.15 rads and 4.4 rads, respectively.[95]

Technetium 99m Dimercaptosuccinic Acid (Tc-99m DMSA)

Tc-99m DMSA localizes to renal cortex at high concentration and has slow urinary excretion rate. About 50% of the injected dose accumulates in the renal cortex at 1 hour. The tracer is bound to the renal proximal tubular cells. In view of the high retention of DMSA in the renal cortex, it has become useful for imaging of the renal parenchyma. For a 6 mCi (11 MBq) dose, the radiation exposures to the kidneys and to the urinary bladder are 3.78 rads and 0.42 rads, respectively.[95]

Fluorine-18 Fluorodeoxyglucose (FDG)

Fluorine-18 Fluorodeoxyglucose (FDG) is the most common positron-labeled radiotracer in positron emission tomography (PET). F-18 labeled deoxyglucose is a modified form of glucose in which the hydroxyl group in the 2-position is replaced by the F-18 positron emitter. FDG accumulates in cells in proportion to glucose metabolism. Cell membrane glucose transporters facilitate the transport of glucose and FDG across the cell membrane. Both glucose and FDG are phosphorylated in the 6-position by the hexokinase. The conversion of glucose-6-phosphate or FDG-6-phosphate back to glucose or FDG, respectively, is effected by the enzyme phosphatase. In most tissues, including cancer, there is little phosphatase activity. FDG-6-phosphate cannot undergo further conversions and is therefore trapped in the cell. FDG is excreted in the urine. The typical FDG dose is 0.144 mCi/kg (minimum 1 mCi, maximum 20 mCi). The urinary bladder wall receives the highest radiation dose from FDG. [96] [97] The radiation dose depends on the excretion rate, the varying size of the bladder, the bladder volume at the time of FDG administration, and an estimated bladder time activity curve. For a typical 15 mCi FDG dose and voiding at 1 hour after tracer injection, the average estimated absorbed radiation dose to the adult bladder wall is 3.3 rads (0.22 rads/mCi).[98] The doses to other organs are between 0.75 and 1.28 rads (0.050–0.085 rads/mCi) for an average organ dose of 1.0 rad.[98]


Glomerular filtration rate and ERPF may be assessed using dynamic quantitative nuclear imaging techniques. The GFR quantifies the amount of filtrate formed per minute (normal: 125 mL/min in adults). Only 20% of renal plasma flow is filtered through the semipermeable membrane of the glomerulus. The filtrate is protein-free and nearly completely reabsorbed in the tubules. Filtration is maintained over a range of arterial pressures with autoregulation. The ideal agent for the determination of GFR is inulin, which is only filtered but is neither secreted nor reabsorbed. [95] [99]

Tc-99m DTPA is often employed to demonstrate renal perfusion and assess glomerular filtration, although 5% to 10% of injected DTPA is protein-bound and 5% remains in the kidneys at 4 hours. A typical imaging protocol includes posterior 5-second flow images for 1 minute followed by 1-minute per frame images for 20 minutes. The GFR may be obtained using the Gates method that employs images of renal uptake during the second through third minute after DTPA administration. Regions of interest (ROIs) are drawn over the kidneys and background activity correction is applied. A standard dose is counted by the gamma camera for normalization. Depth photon attenuation correction is made based on a formula relating body weight and height. A split GFR can be obtained for each kidney, which is not possible with the creatinine clearance method. [95] [99]

The ERPF (normal: 585 mL/min in adults) can be obtained by using OIH and MAG3 imaging.[100] However, OIH has been largely replaced by MAG3 because of MAG3's better imaging characteristics and dosimetry (due to radiolabeling with Tc-99m). Currently MAG3 is the renal imaging agent of choice primarily because of the combined renal clearance of MAG3 by both filtration and tubular extraction, which leads to the ability for obtaining relatively high-quality images even in patients with impaired renal function. The imaging protocol includes posterior 1-second images for 60 seconds (flow study) followed by 1-minute images for 5 minutes and then 5-minute images to 30 minutes. The relative tubular function may be obtained by drawing renal ROIs corrected for background activity. A renogram is constructed to depict the renal tracer uptake over time. The first portion of the renogram has a sharp upslope occurring in about 6 seconds following peak aortic activity (phase I) representing perfusion followed by extension to the peak value representing both renal perfusion and early renal clearance (phase II). The next phase (phase III) is downsloping and represents excretion. Normal perfusion of the kidneys is symmetric (50% +/- 5%). The renogram peak occurs at about 2 to 3 minutes (versus 3 to 5 minutes with DTPA) in normal adults and by 30 minutes, more than 70% of tracer is cleared and present in the urinary bladder ( Fig. 27-24 ). [95] [99] Renal cortical structure can be imaged with DMSA, which correlates strongly with differential glomerular filtration and differential renal blood flow. Imaging is started 90 to 120 minutes after tracer administration, although images can be obtained at up to 4 hours. Planar images are obtained in the anterior, posterior, LAO/RAO, RPO/LPO projections. Single-photon computed tomography (SPECT) is also often obtained. A normal scan shows evenly distributed renal cortical uptake. Normal variations include dromedary hump (splenic impression on the left kidney), fetal lobulation, horseshoe kidney, crossed fused ectopia, and hypertrophied column of Bertin. The renal images also allow accurate assessment of the relative renal size, position, and axis. [95] [99]



FIGURE 27-24  A and B, Normal Tc-99m MAG3 renogram.




Acute kidney injury (AKI/ARF) is characterized as pre-renal, renal, or post-renal in etiology. AKI/ARF is commonly encountered in the hospital setting. In these patients it is most frequently caused by hypotension, dehydration, nephrotoxic drugs, or hypoperfusion of the kidneys.[17] These pre-renal and renal causes account for more than 90% of all cases. The least common type of AKI/ARF, post-renal, is also the most potentially curable. Post-renal AKI/ARF is most often due to urinary tract obstruction or obstructive uropathy. Radiographic evaluation is done to exclude post-renal AKI/ARF in the form of obstructed kidneys. Once post-renal AKI/ARF is excluded, pre-renal and intrinsic causes of AKI/ARF can be managed medically.

Plain films offer little in the assessment of AKI/ARF. Only renal size and the presence or absence of renal stones can be assessed. The IVU plays no role in AKI/ARF as iodinated contrast is required for the study. Ultrasonography is the method of choice in evaluating patients with AKI/ARF. Renal size, echogenicity of the kidneys, cortical thickness, and the presence or absence of hydronephrosis are generally easily imaged.[101] A thin rim of decreased echogenicity may surround the kidneys in patients experiencing kidney injury.[102] For patients with AKI/ARF, the accuracy of ultrasound is greater than 95% in detecting hydronephrosis that is dilatation of the collecting systems and renal pelvis. [103] [104] To make the diagnosis of a post-renal etiology for AKI/ARF, both kidneys should exhibit hydronephrosis.[105] The specific cause may not be elucidated with ultrasound and other methods must be employed, such as CT or MRI.

The principal ultrasonographic finding of hydronephrosis is the separation of the central renal sinus echo complex by a sonolucent fluid-filled renal pelvis, which directly connects to the dilated calyces and infundibula in the more peripheral aspects of the kidney. Hydronephrosis is generally graded by the extent of calyceal dilatation and the degree of cortical thinning. [103] [106] [107] Mild, or grade I, hydronephrosis is diagnosed by noting the fluid-filled pelvicaliceal system causing slight separation of the central renal sinus fat ( Fig. 27-25 ). The calyces are not distorted and the renal cortex appears of normal thickness. In grade II hydronephrosis the pelvicalyceal system appears more distended with greater separation of the central echo complex. The contour of the calyces becomes round, but the cortical thickness is unaltered ( Fig. 27-26 ). With grade III hydronephrosis the calyces are more distended and cortical thinning is recognized. Severe, or grade IV, hydronephrosis exhibits marked dilation of the calyceal system ( Fig. 27-27 ). The calyces appear as large ballooned fluid-filled structures with a dilated renal pelvis of variable size. Cortical loss is evident with the dilated calyces approaching or reaching the renal capsule. Generally speaking, the length and overall size of a hydronephrotic kidney is increased. Longstanding obstruction may, however, result in renal parenchymal atrophy and a somewhat small kidney with marked cortical thinning. The degree of hydronephrosis does not always correlate with the amount of obstruction.



FIGURE 27-25  Mild hydronephrosis—ultrasound. The central echo complex is separated by the mildly distended calyces and renal pelvis. Notice the connection between the calyces and the renal pelvis. The cortex is preserved in thickness and the renal border remains smooth.





FIGURE 27-26  Moderate hydronephrosis—ultrasound. The dilated calyces are rounded and urine filled. The renal pelvis is dilated as well. Again note the connection between the calyces and the renal pelvis. The cortex is mildly thinned and the renal border is smooth. Longitudinal image (A) and transverse image (B).





FIGURE 27-27  Marked hydronephrosis—ultrasound. Longitudinal image of the right kidney demonstrates a large fluid-filled sac with no normal remaining elements of the kidney visible. The cortex is almost gone but the outer border of the kidney remains smooth.



Although hydronephrosis is usually easily diagnosed with ultrasound, it must not be confused with renal cystic disease. With hydronephrosis the dilated calyces have a direct visible communication with the renal pelvis, which is also dilated.[40] In cystic disease, the round fluid-filled cysts have walls with no direct communication evident between each and the renal pelvis. Peripelvic cysts frequently lead to a misdiagnosis of a dilated renal pelvis. Renal artery aneurysm may also be confused with a dilated renal pelvis, but the correct diagnosis can be made with added color Doppler ultrasound.

Nonobstructive hydronephrosis may present a confusing picture ultrasonographically. [108] [109] Grade I hydronephrosis and possibly more severe grades may be seen in patients with no obstructive cause found. To some, mild dilatation of the pelvicalyceal system has been considered a normal variant. Nonobstructive causes of hydronephrosis include increased urine production and flow such as occurs with a diuresis from any cause, pregnancy, acute and chronic infection, vesicoureteral reflux, papillary necrosis, congenital megacalices, over distended bladder, and post obstructive dilatation.[110] In patients with repeated episodes of intermittent or partial obstruction, the calyces become quite distensible or compliant leading to a variable picture of hydronephrosis depending on their state of hydration and urine production. Patients with vesicoureteral reflux also demonstrate distensible pelvicalyceal systems. Duplex Doppler ultrasound has been suggested as an additive means of differentiating obstructive from nonobstructive hydronephrosis. [111] [112] The measurement of resistive indices has been investigated as a means of diagnosing acute renal obstruction.[113] The results have been variable leading to no consistent recommendation. [114] [115]

The use of ultrasound also extends to patients with chronic kidney injury or medical renal disease. Increased cortical echogenicity may be seen in both acute and chronic renal parenchymal disease ( Fig. 27-28 ).[116] The pattern should be bilateral. In chronic kidney injury, the degree of cortical echogenicity correlates with the severity of the interstitial fibrosis, global sclerosis, focal tubular atrophy, and number of hyaline casts per glomerulus.[39] Similar correlation is seen with decreasing renal size. These findings, however, remain nonspecific and renal biopsy is required for diagnosis. Loss of the normal corticomedullary function is seen with increasing cortical echogenicity.[44]Increased cortical echogenicity may also be seen in some patients with AKI/ARF such as glomerulonephritis and lupus nephritis. Sequential studies over time may be used to assess the progression of disease by monitoring the renal size and cortical echogenicity.



FIGURE 27-28  Chronic kidney injury—ultrasound. End-stage renal disease (ESRD) is noted (A, B) with the kidneys being high echogenic relative to the adjacent liver. There are no normal renal structures seen but the kidneys remain smooth in overall contour. Note the two small hypoechoic renal cysts in the surface in A.



The key to the diagnosis of renal parenchymal disease is renal core biopsy and resulting histopathologic diagnosis.[116] Ultrasound facilitates the performance of renal biopsy by demonstrating the kidney and the proper location for biopsy. Ultrasound may also be used to evaluate for complications associated with renal biopsy such as perirenal hematoma.

Computed tomography scanning in AKI/ARF and CRF usually follows ultrasound evaluation that demonstrated bilateral hydronephrosis. Noncontrast CT easily demonstrates the dilated pelvocalyceal systems in the kidney. The parenchymal thickness relative to the dilated collecting systems can be visualized. The urine-filled calyces and pelvis are less dense than the surrounding parenchyma. The dilated ureters may be followed distally to establish the site of obstruction. The cause may be frequently seen, such as the case with pelvic tumors, distal ureteral stones, and retroperitoneal adenopathy or mass. If obstruction is not the cause, other potential etiologies such as cirrhosis and ascites with accompanying hepatic failure may be evident. In CRF, CT scanning will usually demonstrate small contracted kidneys, which may also show evidence of adult acquired polycystic disease ( Fig. 27-29 ). In general, the overall size and thickness of the renal parenchyma appears to decrease with age.[117] For patients with chronic longstanding obstruction as the cause of their kidney injury, CT will generally demonstrate large fluid-containing kidneys with little or no cortex remaining. Autosomal dominant polycystic disease may also be seen with CT ( Fig. 27-30 ). The innumerable cysts are seen throughout the enlarged kidneys. Frequently, some of the cyst walls may contain thin rims of calcification. There may also be variation in the density of the internal contents of the cysts due to hemorrhage or proteinaceous debris. For patients undergoing regular dialysis, iodinated contrast may be given if necessary for CT scans as the material is dialyzable.



FIGURE 27-29  Adult acquired polycystic kidney disease—CT scan. Axial noncontrast (A) and post contrast (B) images. Small kidneys are seen bilaterally with multiple small 1-cm cysts primarily in the cortex.





FIGURE 27-30  Autosomal dominant polycystic kidney disease—CT scan. This noncontrast CT images demonstrates the markedly enlarged kidney bilaterally with multiple low density cysts throughout both kidneys. The little remaining renal parenchyma is noted by the sparse higher density material squeezed by the cysts.



Magnetic resonance imaging is accurate in demonstrating pre-renal and post-renal causes of kidney injury, but unless the cause of injury is secondary to vascular occlusion or collection system obstruction, MRI becomes less specific. MRI is sensitive for the detection of renal parenchymal disease, but the renal parenchymal causes of injury have nonspecific findings and generally require biopsy (figs. 27-31 and 27-32 [31] [32]).[118]



FIGURE 27-31  Renal transplant graft with acute tubular necrosis. A, Axial T2-weighted; B, axial T1-weighted; and C, gadolinium-enhanced T1-weighted images show reversal of the normal corticomedullary differentiation in this patient with biopsy-proven acute tubular necrosis.





FIGURE 27-32  Renal transplant graft with chronic injury due to IgA nephropathy. A, Axial T2-weighted; B, axial T1-weighted; and C, gadolinium-enhanced T1-weighted image demonstrate accentuation of the corticomedullary differentiation.



Initial experience with diffusion weighted MR imaging has demonstrated reproducible information on renal function, with the possibility of determining the degree of dysfunction.[119] No large studies have been performed and further research is required before the usefulness of diffusion imaging is confirmed. Animal research is being performed with the hope of developing therapy for chronic nephropathy. MRI is being used in molecular imaging to follow the targeting of focal areas of glomerular damage by intravenously injected superparamagnetic iron oxide-labeled mesenchymal stem cells.[120]

In kidney injury, glomerular and tubular dysfunctions are reflected by abnormal renal scintigraphy and renograms. Renal uptake of MAG3 is prolonged with tubular tracer stasis and little or no excretion. It has been shown that in patients with acute kidney injury, the demonstration of MAG3 renal activity more than hepatic activity at 1 to 3 minutes indicates likely recovery whereas when renal uptake is less than the hepatic uptake, dialysis may be needed.[121] In chronic kidney injury, there is diminished renal perfusion, cortical tracer extraction, and excretion. However, this imaging pattern is nonspecific and will need to be interpreted in the clinical context.[95]


Although ultrasound is frequently the first imaging method used to detect the obstructed kidney, it usually is unable to establish the cause of the obstruction. Contrast studies, primarily IVU and CT are the methods of choice for the patient with normal renal function. Antegrade or retrograde pyelograms are used as secondary means of assessment. Of these methodologies, CT is the most helpful in establishing the site and cause of unilateral obstruction.

The IVU has been used for years in evaluating the obstructed kidney.[3] The scout film may give a hint as to the cause (i.e., mass in the pelvis). The obstructed kidney is usually larger than the normal other side. The initial nephrogram and appearance of contrast material in the collecting system may be delayed. With time the nephrogram may be increased over that of the normal kidney.[3] Once the collecting system and renal pelvis are opacified with the excreted contrast, they are dilated and distended. The ureters will fill late in relationship to the opposite normal kidney. Delayed images may be required with prone or upright views to identify the site of obstruction. With the IVU, the site of obstruction will be noted, but again the cause may only be inferred; this is also true with the antegrade and retrograde pyelograms.

Contrast-enhanced CT and more specifically, the CT urogram will be most useful in assessing the patient with unilateral obstruction.[51] The findings seen with the IVU are only amplified with the CT urogram. Small differences in the enhancement pattern of the kidney that are not notable on an IVU may be seen with CT ( Fig. 27-33 ). Differential excretion differences are also more sensitively seen on CT. [50] [51] The urine-filled or contrast-filled ureters point to the obstruction. The dilated ureters on the obstructed side may be followed in axial or coronal sections to the cause. The multiple causes of unilateral obstruction may be seen on CT—including both intra- and extra-ureteral cases (Fig. 27-34 ). MRI demonstrates similar findings although its sensitivity and specificity are only now being established.



FIGURE 27-33  Unilateral hydronephrosis—contrast-enhanced CT scan. Axial (A) and coronal (B) nephrographic phase images of an obstructed left kidney. Note the right kidney is in the nephrographic phase whereas the left obstructed left kidney is still in the corticomedullary phase—differential enhancement. In the excretory phase image (C) the right kidney has contrast within the collecting system and the renal pelvis. The left kidney has no contrast in the pelvocalyceal system and only contains non-opacified urine. This patient had lymphoma with retroperitoneal lymph nodes causing the obstruction more distally.





FIGURE 27-34  Unilateral obstruction—contrast-enhanced CT scan. The coronal image demonstrates the differential enhancement between the two kidneys with the moderately dilated renal pelvis and calyces on the right. The large heterogeneous pelvis mass is the source of the obstruction—recurrent rectal carcinoma.



Nuclear medicine assessment by means of diuretic renography may also be used to evaluate for obstructive uropathy. It is a noninvasive procedure and yields excellent results. In general, it is recommended that the patient be well hydrated. In children and in adults with noncompliant bladder, catheterization of the bladder may be used to ensure drainage and reduce back pressure in the urinary system. MAG3 scintigraphy is often employed. Furosemide (Lasix) is administered intravenously (1 mg/kg; higher dose in cases of renal insufficiency) when the renal pelvis and ureter are maximally distended.[122] This may occur in as early as 10 to 15 minutes and as late as 30 to 40 minutes after tracer administration. ROIs are drawn around each renal pelvis with the background regions as crescent shapes lateral to each kidney. Following furosemide administration, rapid emptying of the collecting system with a subsequent steep decline in the renogram curve is compatible with dilatation without obstruction. Obstruction can be excluded if the clearance half time (T1/2) of the renal pelvic emptying is less than 10 minutes. A curve that reaches a plateau or continues to rise after administration of furosemide is an obstructive pattern with a clearance T1/2 of greater than 20 minutes ( Fig. 27-35 ). A slow downslope after furosemide may indicate partial obstruction. An apparent poor response to furosemide may also be seen in severe pelvic dilatation (reservoir effect). Other pitfalls include poor injection technique of either the diuretic or the radiotracer, impaired renal function, and dehydration in which delayed tracer transit and excretion may not be overcome by the effect of a diuretic. Kidneys in neonates (<1 month in age) may be too immature to respond to furosemide and are not suitable candidates for diuretic renal scintigraphy. [95] [123]



FIGURE 27-35  Abnormal Tc-99m MAG3 renogram demonstrating obstructive urinary kinetics with a poor response to furosemide. A, Static and timed images. B, Individual curves for each kidney.




Calcifications may occur in many regions of the kidney.[124] Nephrolithiasis or renal calculi are the most common and occur in the pelvocalyceal system. Nephrocalcinosis refers to renal parenchymal calcification occurring in either the medulla or cortex. These calcifications are usually associated with diseases in which patients have hypercalcemia or hypercalcuria or in conditions with specific pathologic lesions in the cortex or medulla. Nephrocalcinosis may have diffuse or punctate calcifications and is usually bilateral. Some patients with nephrocalcinosis may also develop nephrolithiasis. Calcifications may also occur in vascular structures, particularly in patients with diabetes and advanced atherosclerotic disease. Rim-like calcifications may occur in simple renal cysts and polycystic disease. Renal carcinomas may exhibit variable calcifications as well. Sloughed papilla may also calcify within the calyx. All of these calcifications may be seen on plain films of the abdomen but will be seen to better advantage with noncontrast CT sans of the abdomen ( Fig. 27-36 ).



FIGURE 27-36  Renal stone—plain film. KUB showing a large laminated stone in the renal pelvis of the right kidney. The outline of the normal left kidney can be seen with no calcifications overlying it. The right kidney outline cannot be seen.



Cortical calcification is most often associated with the results of acute cortical necrosis from any cause.[124] Dystrophic calcification develops in the damaged cortex after the episode of acute cortical necrosis. The calcifications tend to be tram track-like and circumferential. Other entities in which cortical calcification are found include hyperoxaluria, Alport syndrome, and rarely, chronic glomerulonephritis. The stippled calcifications of hyperoxaluria may be found in both the cortex and medulla as well as other organs, such as the heart. With Alport syndrome only cortical calcifications are found.

Calcifications in the medulla are much more common than cortical calcifications.[124] The most common cause of medullary nephrocalcinosis is primary hyperparathyroidism. Intratubular deposition of calcium oxalate crystals occurs first with later deposits in the interstitial renal parenchyma. The distribution appears to be within the renal pyramid. The radiological picture may be focal or diffuse, and unilateral or bilateral. Nephrolithiasis also occurs in patients with primary hyperparathyroidism. Nephrocalcinosis occurs in other diseases in which hypercalcemia or hypercalciuria occur. These include hyperthyroidism, sarcoidosis, hypervitaminosis D, immobilization, multiple myeloma, and metastatic neoplasms to name a few. These calcifications are nonspecific and punctate in appearance and are usually medullary in location.

In 70% to 75% of cases of renal tubular acidosis (RTA) there is evidence of nephrocalcinosis. The calcifications tend to be uniform and distributed throughout the renal pyramids bilaterally. With medullary sponge kidney, renal tubular ectasia, small calculi form in the distal collecting tubules probably because of stasis. The appearance is varied from only a single calyx being involved to both kidneys throughout. The calcifications are small, round, and within the peak of the pyramid adjacent to the calyx. Medullary sponge kidney is also associated with nephrolithiasis, as the small calculi in the distal collecting tubules may pass into the collecting systems and ureters resulting in renal colic.[125]

The calcifications that occur in renal tuberculosis are typically medullary in location and may mimic other forms of nephrocalcinosis.[126] Renal tuberculosis begins in the renal cortex and progresses to the medulla. Invasion and erosion of the calyceal system subsequently occurs resulting in spread of the tuberculous infection down the ureters into the bladder. Calcification occurs in the pyramids as part of the healing process. With overwhelming involvement of the kidney, the entire kidney may be destroyed resulting in an autonephrectomy with diffuse, heavy calcification throughout the entire kidney, which is small and scarred. Medullary calcifications are also seen in patients with renal papillary necrosis. With necrosis of the papilla, the material is sloughed into the calyces. Retained tissue fragments may calcify and give the appearance of medullary nephrocalcinosis.

Nephrolithiasis is a common clinical entity. The lifetime risk of developing renal calculi is 12% with males being 2 to 3 times more at risk than females.[127] Most renal stones occur in individuals aged 30 to 60. Renal stone disease is a multifactorial problem with metabolic disorders and other factors, such as geography, diet, family history, diabetes, sedentary lifestyle, and dehydration, contributory to the disorder. Most urinary tract stones are composed of calcium salts of either oxalate or phosphate or a combination of the two. [128] [129] [130] [131] This leads to the dense appearance on radiographs. Stasis contributes to the formation of stones in the urinary tract. Renal colic or flank pain is the most common presenting symptom. Most patients will also have hematuria although it may be absent if there is complete obstruction of the ureters by the obstructing stone. The pain that occurs with a passing renal stone is likely due to the distension of the tubular system and renal capsule of the kidney and the peristalsis associated with ureteral contractions as the stone moves distally.

Plain films of the abdomen require a stone that is densely calcified and of sufficient size to be visible (see Fig. 27-36 ). Frequently overlying bowel gas and feces may make visualization difficult. Costal cartilage calcifications in the upper abdomen may be confused with renal calculi as may gallstones in the right upper quadrant. For years the IVU has been the method of choice for the assessment of the patient with renal colic. [132] [133] After the injection of IV contrast media, there is an unequal nephrogram with a delayed appearance on the affected sides. Once the nephrogram appears, it may also be prolonged and increase in density with time, specifically with complete obstruction caused by a ureteric stone. The excretion of contrast into the collecting system is usually delayed and there is dilatation of the pelvocalyceal system. Delayed images up to 24 hours may occasionally be necessary to visualize the contrast-filled dilated collecting systems, pelvis, and ureter to the point of obstruction by the calculus. When the pelvocalyceal system is contrast filled and the ureter is not, upright or prone films may help fill the ureter with contrast. The injection of contrast, being a fluid load, may assist the stone in passage through the ureters into the bladder.

Most urinary calculi that are 4 mm or smaller will pass with conservative treatment.[134] The larger the stone the more likely other measures will be necessary in order to treat the stone and associated obstruction. Extracorporal shockwave lithotripsy (ESWL) is the method of choice for treating larger stones. Success rates are best for stones in the renal pelvis and kidney.[135]

Ultrasound assessment has also been used in the evaluation of renal colic.[136] This is quick and usually easily performed examination. One is looking for the effects of a passing renal stone, which is obstruction. Unilateral hydronephrosis may be seen although the examination may be normal early in the passage of a renal stone. Renal stones may be visualized within the kidney as hyperechoic foci with distal acoustic shadowing or reverberation artifacts ( Fig. 27-37 ).[136] Ureteric stones are rarely seen due to overlying bowel gas and stone. Distal ureteral stones near the uretovesical junction may be visualized through the urine-filled bladder transabdominally. Transvaginal and transperineal ultrasound has also been suggested as a method for evaluating for distal ureteral stones. Ultrasound may demonstrate an absent ureteral jet in the bladder on the side in which a stone is being passed. Doppler ultrasound and assessment of the peripheral vasculature resistance may occasionally be helpful in pointing to the affected kidney, but the study results have been variable.[113]



FIGURE 27-37  Renal stone—ultrasound. Longitudinal image (A) and color Doppler image (B) demonstrate an echogenic focus at the corticomedullary junction. Not all stones show shadowing but in this case reverberation artifact can be seen on the color Doppler image helping make the diagnosis.



Noncontrast CT scanning of the abdomen and pelvis has emerged as the standard for evaluation of patients with renal colic. [137] [138] [139] The sensitivities for CT of 96% to 100%, specificities of 95% to 100%, and accuracies of 96% to 98%, non-enhanced CT has supplanted the plain film, IVU, and US. [138] [140] [141] [142] Comparing noncontrast CT and the IVU, CT performs much better with sensitivity of 94% to 100% and specificity of 92% to 100% versus the IVU with sensitivity of 64% to 97% and specificity of 92% to 94%.[138] Also, when noncontrast CT was used as the reference standard comparing US, a sensitivity of 24% and specificity of 90% was found for US. [143] [144] As CT scanning uses x-ray radiation for the study, US examination should be reserved for the pediatric population and pregnant women. Alternative diagnosis is made in patients with “renal colic” in 9% to 29% of cases when noncontrast CT is used for evaluation.[145]

Nonenhanced CT scans are performed from the top of the kidneys to below the pubic symphysis. No preparation is needed. Intravenous contrast is rarely needed. The studies are performed using 3 mm collimation or less with the slices reconstructed contiguously or slightly overlapped. [146] [147] [148] The images should be viewed on a monitor as axial images with multiplanar reconstructions (MPR) used as an adjunct. Virtually all renal stones are denser than the adjacent soft tissues ( Fig. 27-38 )[149]; exceptions are renal stones associated with Indinavir, a protease inhibitor used in the management of AIDS, and very small uric acid stones (<1–2 mm). [150] [151] As expected, calcium oxalate and calcium phosphate stones are the most dense. [129] [130] Matrix stones, which are rare, may also be relatively low in density, but they usually contain calcium imparities that make them visible. [128] [131]



FIGURE 27-38  Renal stones—noncontrast CT scan. Axial image (A) and coronal image (B) demonstrate 4 mm to 5 mm stones in the upper and lower poles of the left kidney. There are no signs of obstruction.



Calculi appear as calcifications within the urinary tract. The most common locations for obstruction to occur are at the ureteropelvic junction, at the pelvic brim where the ureters cross over the iliac vessels, and at the uretovesical junction. The diagnosis is made on the CT scan by demonstrating the calcified stone within the urine-filled ureters ( Fig. 27-39 ).[146] Secondary signs may be present to assist in the diagnosis.[140] Hydronephrosis and hydroureter to the point of the stone may be visible (see Fig. 27-39 ). Asymmetric perinephric and periureteral stranding may also be seen related to forniceal rupture and urine leak ( Fig. 27-40 ).[152] The density of the involved kidney may be less than the opposite normal side due to increased interstitial fluid and edema. [153] [154] The affected kidney may also be larger than the normal kidney. At the point of obstruction, the stone may be seen within the ureter with soft tissue thickening of the ureteral wall at that level. This is likely due to edema and inflammation associated with the passage of the stone. Noncontrast CT has the advantage as well of assessing the overall stone burden of the patient, not just the passing stone. Also the size may be accurately measured allowing for treatment decisions to be made. [134] [155] [156] Distal ureteral stones may occasionally be confused with phleboliths, which are common in the pelvis (see Fig. 27-40 ). Multiplanar imaging coronal images of the ureters down to the level of the stone may be helpful. Also, close inspection of phleboliths frequently demonstrates a small soft tissue tag leading to the calcification—the comet tail sign.[157] Contrast material injection may occasionally be necessary in confusing or difficult cases. Also, it may be used in complicated cases in which the patient is febrile and pyelonephritis or pyohydronephrosis is suspected.



FIGURE 27-39  Ureteral stone—noncontrast CT scan. (A) A 5 mm to 6 mm right mid-ureteral stone is noted. (B) Axial images of the middle portion of the kidneys reveals the urine-filled right renal pelvis and a slightly less dense kidney when compared with the left. These are signs of obstruction.





FIGURE 27-40  Ureteral stone—noncontrast CT scan. Axial images of the kidneys (A) show perinephric and peripelvic stranding and fluid on the right caused by forniceal rupture and leak of urine due to the distal obstructing stone at the right ureterovesical junction (B). Note the phlebolith on the right posterior to the bladder and lateral to the seminal vesicle—a common pitfall.



Computed tomography is more sensitive for the evaluation of renal and collecting system calcifications, especially in the absence of urinary tract obstruction. In the evaluation of acute stone disease, MRI is not the examination of first choice, but is a suitable alternative for selected patients.[158] Stones are difficult to identify in non-dilated systems, even in retrospect. When stones are seen on MRI they are seen as black foci on both T1- and T2-weighted sequences. Stones become more conspicuous in a dilated collecting system ( Fig. 27-41 ); however, a non-enhancing filling defect is a nonspecific finding. Blood, air, or debris may have the same appearance. If stones or other calcifications are a concern, noncontrast CT is the examination of choice for improved conspicuity ( Fig. 27-42 ).



FIGURE 27-41  Renal stones. (A) Calcification well seen on CT (arrowhead) is (B) difficult to demonstrate on MRI (arrow), even in retrospect. C, A stone (arrowhead) is more conspicuous when it is located within a mildly dilated collection system.





FIGURE 27-42  Staghorn calculus. (A) MRI and (B) CT demonstrating large pelvic calculus with associated left renal atrophy. Even large stones may be difficult to recognize on MRI. Calcifications are more conspicuous on CT.



When iodinated contrast is contraindicated or when reduction of radiation exposure is desired, MR urography (MRU) can be used to determine the etiology and location of an obstructing process ( Fig. 27-43 ). MRU is highly accurate in demonstrating obstruction whether the process is acute or chronic.[158] Acute obstruction may be associated with perinephric fluid, which is well demonstrated on T2-weighted sequences. [158] [159] However, perinephric fluid is a nonspecific finding and can be found associated with other renal pathology.



FIGURE 27-43  Magnetic resonance urogram reconstructions demonstrating a non occluding distal ureteral stone (arrow). A-C, 3D post processing techniques are used to mimic IV urography. D, Post contrast, axial imaging demonstrates a stone within the lumen of the distal ureters.



Although MRI is not the imaging modality of choice for acute renal trauma evaluation, MRI is useful in evaluating the patient who is recently post op for renal stone disease, especially in the patient with impaired renal function. MRI has been reported as being more accurate than CT in differentiating perirenal and intrarenal hematomas (Figs. 27-44 to 27-46 [44] [45] [46]).[160] With contrast, MRI can also demonstrate damage to the collecting system and areas of ischemia without the risk of nephrotoxicity.



FIGURE 27-44  Subcapsular hematoma post lithotripsy. A, Coronal T2-weighted sequence demonstrating high-signal intensity blood contained by left renal capsule (arrowheads)B, Axial T1-weighted and (C) gadolinium-enhanced T1-weighted image show mass effect on left kidney (arrowheads) caused by a subcapsular hematoma. The signal intensity is consistent with intracellular methemoglobin.





FIGURE 27-45  Post traumatic subcapsular hematoma. A, Sagittal T2-weighted and (B) post contrast T1-weighted images show a subcapsular hematoma (arrowheads) with signal intensity consistent with extracellular methemoglobin. This hematoma is older than the one shown in Figure 27-44 .





FIGURE 27-46  Hematoma status post surgical removal of staghorn calculus. A, T2-weighted, axial; B, T1-weighted, axial; and C, T1-weighted post contrast, axial images show an intrarenal hematoma (arrows) at the site of incision plane. This extends into the renal pelvis. No urine extravasation was demonstrated.




Acute pyelonephritis is typically a clinical diagnosis based on signs and symptoms of flank pain, tenderness, and fever with accompanying laboratory findings of leukocytosis, pyuria, positive urine culture, and occasionally bacteremia and hematuria.[161] Most cases of acute pyelonephritis occur by the ascending route from the bladder.[161] Vesicoureteral reflux is viewed as the major cause. The gram negative bacteria are transported to the renal pelvis where intrarenal reflux occurs with the bacteria traversing the calyceal system to the ducts and tubules within the renal pyramid. With the bacteria within the tubules, there is a leukocyte response. Enzyme release results in destruction of tubular cells with subsequent bacterial invasion of the interstitum. The resultant inflammatory response involves both the interstitum and tubules. As the infection progresses it spreads throughout the pyramid and to the adjacent parenchyma. The inflammatory response leads to focal or more diffuse swelling of the kidney. Vasoconstriction of the involved arteries and arterioles is noted. Without adequate treatment there is necrosis of the involved regions and micro-abscess formation. These may coalesce into larger macro-abscesses, which tend to be surrounded by a rim of granulation tissue.[162] Perinephric abscess results from the rupture of an intrarenal abscess through the renal capsule or the leak from pyonephrosis, an infected and obstructed kidney. The overall distribution in the kidney is usually patchy or lobar although sometimes diffuse.[161] Subsequent scarring of the kidney after treatment reflects the magnitude of the infection and tissue destruction that occurred. Reflux is most common in childhood but may occur in adults with lower urinary tract infections or neurogenic bladders.

Hematogenous infection occurs initially in the cortex of the kidney. It eventually involves the medulla. It does not tend to be lobar or pyramidal in distribution. The areas of involvement are usually round, peripheral, and frequently multiple. These infections are usually caused by gram positive bacteria, such as staph aureus and streptococcus species. Bloodborne infection is less common than ascending infections and is usually seen in IV drug abusers, immunocompromised patients, or patients with a source of infection outside the kidney such as heart valves or teeth.

In the patient with AIDS, urinary tract infections are quite common.[163] The infections are frequently hematogenous with unusual organisms such as pneumocystitis carinii, cytomegalovirus, and mycobacterium avium-intracellulare (MAI). The infections may also be seen in other abdominal organism—liver, spleen, and adrenals. [164] [165]

Imaging is rarely used or needed in the uncomplicated case of acute pyelonephritis. It is reserved for the patient who is not responding to conventional antibiotic treatment, patients with an unclear diagnosis, patients with coexisting stone disease and possible obstruction, patients with diabetes and poor antibiotic response, and immunocompromised patients. Imaging is used to assist in confirming the diagnosis and determine the extent of the disease. It is also used in assessing complications of acute pyelonephritis including renal abscess, emphysematous pyelonephritis, and perinephric abscess.

Renal abscess formation is more common with hematogenous infection, although it does occur with ascending infection.[161] Emphysematous pyelonephritis is a severe necrotizing infection of the renal parenchyma usually caused by gram negative bacteria (E. coli, Klebsiella pneumoniae, Proteus Mirabilis).[166] Ninety percent of those with emphysematous pyelonephritis have un-contributed diabetes.[167] It is characterized by severe acute pyelonephritis, urosepsis, and hypotension. It is felt that the gas found in the renal parenchyma is formed due to the high levels of glucose in the tissue by fermentation with the production of CO2. The gas may also be seen in the pelvocalyceal system or perinephric space (or both). Xanthogranulomatous pyelonephritis is a complication of longstanding obstruction and chronic infection, usually with Proteus or E. coli.[168] There is destruction of the renal parenchyma with replacement by vast amounts of lipid laden macrophages. Staghorn calculi are commonly encountered. The kidney is usually barely functional or nonfunctional. The destruction is typically global, but may involve only a portion of the kidney.

Renal tuberculosis occurs by hematogenous spread of pulmonary infections. The genitourinary track is the second most common site of involvement. Evidence of previous pulmonary tuberculosis is found in 70% to 75% of patients with genitourinary tuberculosis. Only 5% may have active tuberculosis. Renal involvement is bilateral with the findings being determined by the extent of the infection, stage of the infection, and host response. Calcified granuloma may be found within the cortex or medullar, papillary necrosis may be seen, and hydrocalyx with infundibular strictures may develop ( Fig. 27-47 ). The kidney may become focally or globally scarred as the disease progresses. There may be areas of nonfunction with dystrophic calcifications. In its end stage, a small scarred kidney with bizarre calcifications may be found—the so-called autonephrectomy. [126] [169]



FIGURE 27-47  Renal tuberculosis—contrast-enhanced CT scan. Axial (A) and coronal (B) images show the destroyed right kidney due to renal tuberculosis. Parenchymal calcifications are present with dilated calyces due to the attenuated and truncated renal pelvis and ureter.



In uncomplicated acute pyelonephritis the IVU may be normal in up to 75% of cases. [162] [170] When present, the findings are usually unilateral and may be segmental. The findings include renal enlargement, altered nephrogram, decreased concentration of contrast material, and delayed appearance of contrast in the calyces. The calyces and renal pelvis may be attenuated or mildly dilated as is the ureter. The kidney may be globally enlarged due to edema or may show a contour bulge with more focal involvement. The nephrogram may be diminished in intensity or even absent when compared to the opposite normal side. Delayed images may occasionally show a prolonged nephrogram on the affected side. The appearance time of the excreted contrast in the calyces may be delayed segmentally or globally and the overall density of the contrast may be diminished compared with the opposite side. The affected region will show attenuated calyces due to the edema although on occasion the calyces may be dilated. Dilatation of the pelvocalyceal system and ureter is due to atony or poor peristalsis with the system. This is a form of nonobstructive dilatation or hydronephrosis. The IVU usually will return to normal within 3 to 6 weeks of the occurrence of the episode of acute pyelonephritis.

Ultrasound is normal in the majority of patients with acute pyelonephritis. When the examination is abnormal, the findings are often nonspecific. Ultrasound is performed to look for a cause for acute pyelonephritis, such as obstruction or renal calculi, and to search for complications. Altered parenchymal echogenicity is the most frequent finding with loss of the normal corticomedullary differentiation. The echogenicity is usually decreased or heterogeneous in the affected area ( Fig. 27-48 ). There may be focal or generalized swelling of the kidney. Power Doppler imaging may improve sensitivity in demonstrating focal hypoperfusion, but this is nonspecific. In patients with AIDS, renal nephropathy is found to have increased cortical echogenicity with loss of the corticomedullary differentiation ( Fig. 27-49 ).[165] Renal size is also increased and this is generally a bilateral process.



FIGURE 27-48  Acute pyelonephritis—renal ultrasound. The hypoechoic region in the upper pole represents an area affected by acute pyelonephritis. The surrounding parenchyma is somewhat distorted with loss of the normal corticomedullary junction.





FIGURE 27-49  AIDS nephropathy—ultrasound. Longitudinal image of the right kidney. The kidney is of normal size to slightly increased size. The corticomedullary distinction is lost with diffuse increased cortical echogenicity.



Computed tomography is the most sensitive and specific means to image the patient with acute pyelonephritis.[170] Although the study may be normal in mild, uncomplicated pyelonephritis, it is still the most effective means of assisting in establishing the diagnosis, judging the extent, and evaluating for complications. Generally, noncontrast and post-contrast scans are used with the contrast-enhanced study being the most effective. The nephrographic phase of the CT scan is best for imaging the patient with acute pyelonephritis ( Fig. 27-50 ). Wedge-shaped areas of decreased density extending from the renal pyramid to the cortex are most characteristic.[170] The nephrogram may be streaky or striated in a focal or global manner ( Fig. 27-51 ).[171] There may be focal or diffuse swelling of the kidney.[172] The areas of involvement may appear almost mass-like (see Fig. 27-50 ). The changes in the nephrogram are related to decreased concentration of contrast media in the tubules with focal ischemia. There is also tubular destruction and obstruction with debris. There is usually a sharp demarcation with the normal parenchyma that continues to enhance normally in the nephrographic phase. There is soft tissue stranding and thickening of Gerota's fascia due to the adjacent inflammatory process (see Fig. 27-51 ).[162] There may be thickening of the walls of the renal pelvis and proximal ureter. Effacement of the calyces and renal pelvis may be seen. Mild dilation may also be occasionally noted. The kidney may have a single focal area of involvement or multiple areas with similar findings. With hematogenous-related pyelonephritis the early findings tend to be multiple, round cortical regions of hypodensity that become more confluent and involve the medulla with time.[172] These findings will persist for weeks despite successful treatment with antibiotics.



FIGURE 27-50  Acute pyelonephritis—contrast-enhanced CT scan. Axial (A) and coronal (B) images. The left kidney shows multiple areas of involvement. The hypodense region in the mid kidney appears almost mass-like (A, B). A striated nephrogram is seen in the region of involvement in the upper pole (B).





FIGURE 27-51  Acute pyelonephritis—contrast-enhanced CT scan. The heterogeneous CT nephrogram shows the diffuse involvement of the right kidney. There is stranding and some fluid seen in the perinephritic space with thickening of Gerota's fascia.



Complications of acute pyelonephritis include renal abscess, perinephric abscess, emphysematous pyelonephritis, and xanthogranulomatous pyelonephritis. All of these entities are imaged best with cross-sectional imaging techniques, most specifically CT. Renal abscess results from severe pyelonephritis with coalescence of necrotic regions and microabcesses. They occur two to three times more frequently in diabetic patients.[167] The findings on IVU are nonspecific with renal mass being suggested by the contour bulge of the kidney and the hypodense region in the nephrogram. Adjacent calyces are not visualized due to edema or their destruction by the abscess cavity. Ultrasound assessment reveals an anechoic or hypoechoic mass with irregular walls. There is usually debris within the abscess leading to some low level echoes. There is usually poor through transmission. Highly echogenic foci within an abscess may represent microbubbles or gas. The wall may demonstrate increased vascular on color Doppler sonography. CT findings in renal abscess include a reasonably well-defined mass with a low density central region and a thick irregular wall or pseudocapsule ( Fig. 27-52 ).[170] There is variable enhancement seen in the region adjacent to the abscess depending on the amount of inflammation. Mature abscesses may demonstrate a more sharply demarcated border with peripheral rim enhancement. Gas may be seen within the abscess.



FIGURE 27-52  Renal abscess—contrast-enhanced CT scan. Axial image (A) demonstrates the hypodense abscess in the right kidney with extension into the perinephritic space and the right flank. Axial image (B) with the patient in the decubitus position reveals the method of diagnosis—needle aspiration. A drainage catheter was subsequently placed for treatment.



Perinephric abscess formation is the result of renal abscesses rupturing through the renal capsule or emphysematous pyelonephritis extending through the capsule into the perinephric space.[172] The IVU may demonstrate on the nephrogram lucency around the kidney. The kidney is usually poorly functioning so complete assessment is difficult. Ultrasound assessment may show fluid or debris (or both) in a localized or generalized fashion around the kidney. With CT, the complete extent of perinephric involvement may be seen. Subcapsular extension may be separated from perinephric involvement. Generally, there is heterogeneous fluid density material seen in the perinephric space. It may contain gas as well. Extension within the retropertoneum is easily recognized into the psoas muscle and adjacent structures (see Fig. 27-52 ). With psoas involvement, it may extend into the pelvis and as far as the groin following the course of the iliopsoas muscle.

With emphysematous pyelonephritis, gas is seen within the renal parenchyma.[166] If the gas is extensive enough, it may be visible on plain films or KUB. The gas is usually mottled, bubbly, or streaky in appearance and may be seen in the areas over the kidneys. With gas in the pelvicalyceal system, it may be seen as the gas-filled outline of the renal pelvis and collecting systems. The IVU contributes little to the diagnosis as the involved kidney is usually nonfunctional. Nephrotomography may displace the gas within the kidney to better advantage. Ultrasound may suggest the diagnosis of emphysematous pyelonephritis by the demonstration of gas within the kidney.[173] With gas present there will be acoustic shadowing in the involved region with adjacent microbubbles causing ring down artifacts. CT is most specific in that the gas may be visualized and the extent of involvement determined.[174] There is generally extensive parenchymal destruction with streaks of gas or mottled collections of gas within the kidney ( Fig. 27-53 ). There is little or no fluid seen. The gas is seen dissecting through the parenchyma in a linear focal or global manner. The gas usually radiates along the pyramid to the cortex. It may extend through into the perinephric space. Emphysematous pyelitis represents gas in the pelvocalyceal system only.[175] It is best diagnosed with CT where parenchymal gas is easily seen. The diagnosis distinction is important in that emphysematous pyelitis carries a less grave prognosis.



FIGURE 27-53  Emphysematous pyelonephritis—contrast-enhanced CT scan. A noncontrast image (A) and contrast-enhanced image (B) demonstrate gas in the renal parenchyma with extension into the perinephritic space. The nephrogram is striated throughout. Global involvement of the kidney is frequent.



Xanthogranulomatous pyelonephritis is an end-stage condition resulting from chronic obstruction with longstanding infection.[168] The plain film or KUB will show a staghorn calculus or large calcification overlying the region of the kidney with a large mass filling the space. An enlarged kidney with loss of identifiable landmarks is seen with ultrasound. The renal sinus echoes are lost. There is usually a large calculus or staghorn calculus filling the space with adjacent debris-filled hypoechoic regions ( Fig. 27-54 ). At times it appears as a large heterogeneous mass. CT defines the extent and adjacent organ involvement best in patients with xanthogranulomatous pyelonephritis. The CT findings include an enlarged but generally reniform mass filling the perinephric space. [168] [176] Calcification, specifically calculi and staghorn calculi are found in 75% of cases. There is absent or markedly decreased excretion seen in 85% of cases and the involved region appears as a mass in more than 85% of cases.[168] In less than 15% of cases the process is focal with normally functioning area of the kidney remaining. The kidney appears enlarged and usually nonfunctional with multiple round hypoattenuating regions with adjacent calcification. There is frequent perinephric extension. Fistulas may occur to adjacent structures with adenopathy noted in the retroperitoneum.



FIGURE 27-54  Xanthogranulomatous pyelonephritis—contrast-enhanced CT scan. A large staghorn calculus fills the renal pelvis and collecting systems in the left kidney. Much of the remainder of the kidney is replaced by hypodense material—the xanthogranulomatous infection—within the calyces and parenchyma with some minimal remaining enhancement of the cortex.



Chronic pyelonephritis is usually associated with vesicoureteral reflux occurring in childhood.[169] The kidney has focal scars that are associated with calyceal dilatation. The scarring is often separated by normal regions of the kidney and normal appearing calyces. When there is global involvement the kidney may be small. The IVU demonstrates dilated or ballooned calyces that extend to the cortical surface, which is thinned. The outline of the kidney will be distorted. One or both kidneys may be involved. With ultrasound the kidneys have irregular outlines with regions of cortical loss. Underlying dilated calyces may be visible. The regions of scarring may be echogenic compared with the adjacent normal kidney. CT scans will demonstrate abnormal architecture within the kidney.[172] Nephrographic phase images reveal the regions of cortical loss with the involved dilated calyces extending to the capsular surface. Variable dilatation of the calyces is seen. Again, the process may be unilateral or bilateral. Excretory phase images will best delineate the extent of involvement especially when presented in a coronal format.

Magnetic resonance imaging is comparable to contrast-enhanced CT for the evaluation of pyelonephritis, abscess, and post infectious scarring.[177] Because CT is more sensitive for the evaluation of stones and gas, MRI is reserved for those patients with contraindications to iodinated contrast or radiation exposure ( Fig. 27-55 ).



FIGURE 27-55  Renal tuberculosis. A and B, T2-weighted images demonstrate asymmetrical cortical thinning and focal areas of increased signal intensity in the distribution of the medullary pyramids. C, Post contrast T1-weighted image shows absence of enhancement consistent with granulomas with caseous necrosis. D, T2-weighed image after treatment shows distorted, dilated calyces containing debris. Right hydronephrosis is seen due to a distal ureteral stricture.



Acute pyelonephritis is associated with fever, flank pain, leukocytosis, and pyuria. Radiolabeled leukocyte (e.g., In-111 WBC) and gallium-67 citrate scans can be helpful in identifying acute pyelonephritis. However, these methods have the drawbacks of extended imaging time (more than 24 hours) and higher radiation exposure. Cortical imaging with DMSA has been shown to be highly sensitive for detecting acute pyelonephritis in the appropriate clinical setting.[178] Acute pyelonephritis demonstrates segmental regions of decreased tracer uptake in oval, round, or wedge pattern. There may also be diffuse generalized decrease in renal uptake, which in association with normal or slightly enlarged kidney is suspicious for an acute infectious process. The pathophysiologic basis for decline in DMSA cortical uptake in infection is related to diminished tracer delivery to the infected area and to direct infectious injury to the tubular cells compromising their function and tracer uptake. A wedge-shaped cortical defect with regional decrease in renal size is compatible with post-infectious scarring. Renal infarcts may also have similar appearance. [95] [99]


Renal masses are quite common with simple renal cysts found in more than 50% of patients over the age of 50. The vast majority of renal masses are simple cysts with solid renal masses, such as renal cell carcinoma, in the minority. Renal masses produce variable findings in the kidney depending on their location. The contour of the kidney may be deformed, calyces displaced or splayed, density of the kidney altered, or the axis of the kidney changed. For years, the IVU was the method of choice for detection of renal masses. Studies have shown it is the low sensitivity for detection of renal masses especially those less than 3 cm in size.[179] A normal IVU does not exclude a renal mass. Using CT as the “gold standard”, IVU detected 10% of masses less than 1 cm, 21% of masses 1 cm to 2 cm in size, 52% of those 2 cm to 3 cm in size and 85% of renal masses greater than 3 cm.[179] Ultrasound fared better but still detected only 26% of masses less than 1 cm, 60% of those 1 cm to 2 cm in size, 82% of masses 2 cm to 3 cm, and 85% of renal masses greater than 3 cm.[179] The findings on IVU are frequently nonspecific and further imaging is required to accurately characterize the renal mass. Ultrasound, CT, and MRI are needed to differentiate solid from cystic renal masses.

Simple renal cysts are commonly encountered with all imaging studies today. They are rarely seen in individuals under the age of 25, but are seen in with great frequency in individuals over the age of 50. Typically, renal cysts are asymptomatic, cortical in location, and may be single or multiple. The cause is unknown. The plain film (KUB) is rarely helpful unless the cyst is quite large. A thin peripheral curvilinear rim calcification may be seen in 1% to 2% of cases. The findings on IVU depend on the position in the kidney and associated deformity of the renal contour and splaying of the pelvocalyceal system. Nephrotomography will yield a well outlined, homogenous lesion that is less dense than the surrounding kidney ( Fig. 27-56 ). The wall of the cyst will be paper thin with a sharp, clear-cut demarcation with the adjacent kidney. The interface with the kidney when a cyst lies on the surface will be beak-like. The calyces will be displaced or splayed.



FIGURE 27-56  Renal mass—nephrotomogram. The left kidney reveals a slightly hypodense mass projecting off the lateral border of the kidney. This proved to be a renal cyst with subsequent imaging.



Ultrasound is an excellent means of diagnosing a simple renal cyst if all imaging criteria are met.[40] The lesion in the kidney will be round or oval and must be anechoic (no echoes within) ( Fig. 27-57 ). It must be well circumscribed with a smooth wall. There must be enhanced through transmission of the sound beyond the cyst with a sharp interface of the back wall with the renal parenchyma. Thin septa may be seen within the cyst, but no nodules on the wall. If all criteria are met, the diagnosis is sound. If there is any deviation from the findings discussed earlier, further imaging with CT or MRI is necessary.



FIGURE 27-57  Renal cyst—ultrasound. A large anechoic renal mass is seen projecting off the lateral border of the right kidney. The cyst features include a well-circumscribed lesion with a sharp back wall and increased through transmission. There are no internal echoes or nodularity and the wall is smooth. There is a clear interface with the kidney.



Computed tomography is the method of choice for characterizing and differentiating renal masses. [180] [181] [182] A simple renal cyst will appear as a well-circumscribed, round, water-dense lesion within the kidney ( Fig. 27-58 ). The CT numbers of the cyst will be near zero. There will be no significant enhancement of the contents after the injection of contrast media. The CT numbers may vary slightly from water density, but no more than 10-15 Hounsfield units. The cyst must be uniform throughout with no measurable wall. The interface with the adjacent parenchyma must be sharp. The margins must be smooth with no perceptible nodules. Thin rim-like calcification may be seen. Occasionally, “high density” cysts may be encountered with CT numbers of 50 to 80 range. These are cysts containing hemorrhage or proteinaceous debris. They demonstrate no wall nodularity and again have no significant enhancement after contrast injection. They are common in polycystic kidneys.



FIGURE 27-58  Renal cyst—CT scan. Axial noncontrast (A) and post contrast (B) images. The cyst is well circumscribed with no enhancement. It displays water density with CT numbers of 0-5. There is a sharp interface with the kidney and no perceptible wall. There are no nodules seen and it is uniform throughout.



Polycystic renal disease is classified as infantile, adult, or acquired. The infantile form is inherited as an autosomal recessive disorder.[183] It has a variable presentation with severe kidney injury being found with a neonatal presentation and congenital hepatic fibrosis and hepatic failure when presenting in older children. Organomegaly is common with bilateral symmetrical renal enlargement. The IVU yields poor visualization of the kidneys due to renal impairment with a prolonged, mottled nephrogram with a striated or streaky appearance. Ultrasound reveals enlarged, diffusely hyperechoic kidneys due to the abnormality involved, that of dilated, ectatic collecting tubules.[184]There is loss of the corticomedullary differentiation as well. CT and MRI are rarely used as the diagnosis is made clinically with the associated ultrasound findings.

Autosomal dominant polycystic disease (ADPK) is the adult form.[185] The plain film will be normal early in the disease process, but as the cysts increase in size so does the overall renal size. When advanced, there will be large bilateral masses present with occasional curvilinear calcifications in the wall of some of the cysts. The IVU will demonstrate multiple lucencies throughout the kidneys, a Swiss-cheese appearance. When renal function is still normal there is extensive splaying and distortion of the pelvicalyceal system. Ultrasound reveals enlarged kidneys bilaterally, which are markedly lobulated containing multiple sonolucent areas of varying size throughout the kidneys.[186]

Computed tomography in ADPK yields enlarged, lobulated kidneys with a myriad of cysts of varying size throughout ( Fig. 27-59 ). One kidney may be more involved than the other. The cysts may have calcifications with the wall. It is not uncommon to encounter cysts with varying density due to episodes of hemorrhage that occur within the cysts. A fluid level may be seen due to the presence of debris or hemorrhage within some of the cysts. In the excretory phase there is marked distortion of the calyces. The extent of renal involvement by ADPK is better appreciated in CT than US or IVU. Cysts may be found in the lever, spleen, and pancreas as well.



FIGURE 27-59  Autosomal dominant polycystic kidney disease—CT scan. Axial noncontrast (A), nephrographic phase (B), and excretory phase (C) images. The equally enlarged kidneys are seen bilaterally with the multiple varying sized cysts involving both kidneys. The calyces are splayed apart and distorted in the excretory phase image (C). Note the multiple small cysts also present in the involved liver.



Adult acquired polycystic kidney disease (AAPKD) occurs in patients with kidney injury undergoing continuous peritoneal dialysis or hemodialysis.[187] The longer the patient has undergone dialysis, the higher the likelihood of AAPKD.[188] Most patients will have undergone dialysis for several years before it is discovered.[189] The cysts are generally quite small (0.5 cm to 2 cm in most). Calcification may occur in the wall. Plain films and IVU play no role due to impaired renal function. Ultrasound reveals small, shrunken kidneys with anechoic or hypoechoic regions representing the cysts. The findings are usually bilateral. CT or MRI will show the small bilateral kidneys with cysts of varying size but usually in the 1 cm to 2 cm range (see Fig. 27-29 ). [190] [191] These cysts must be closely evaluated for solid components as carcinomas and adenomas occur with increased frequency in these patients. Solid lesions less than 3 cm in size may represent either adenomas or renal cell carcinomas, whereas most lesions greater than 3 cm are renal cell carcinomas. [192] [193] Screening for AAPKD is usually done with ultrasound every 6 months, with CT or MRI reserved for patients with questionable or solid lesions.[194]

Medullary sponge kidney, or renal tubular ectasia is a non-hereditary developmental disorder with ectasia and cystic dilation of the distal collecting tubules. The cystic spaces predispose to stasis leading to stone formation and potential infection. Involvement is usually bilateral although not always symmetric with as few as one calyx involved. The kidneys are typically normal sized with a medullary nephrocalcinosis picture when the small stones are present.[125] The IVU reveals linear or round collections of contrast extending from the calyceal border forming parallel brush like striations. With more severe involvement the cystic dilatations may appear grape-like or bead-like. CT is an excellent method for demonstrating the calculi, although the striations or cystic dilatation may be difficult to visualize even with thin section excretory phase imaging.

Multicystic dysplastic kidney is an uncommon, congenital, non-hereditary condition. It is usually unilateral and affects the entire kidney. Rarely only a portion of the kidney is involved. The affected kidney is nonfunctional on IVU. Ultrasound reveals multiple anechoic cystic structures of varying size replacing the kidney with no normal parenchyma seen. Calcification in the wall of the cystic spaces may be seen. CT demonstrates multiple fluid-filled structures filling the renal fossa. Septa and some rim calcifications may be visible. The density of the fluid is usually that of water (≈0) or slightly higher. There is no contrast enhancement seen with the injection of IV contrast. The renal artery to the affected size is not visible. It may be difficult to differentiate from severe hydronephrosis if no cyst walls or septa are visible.

Small cortical cysts may be seen in some hereditary syndromes (i.e., tuberous sclerosis). These cysts are typically multiple and very small (i.e., a few millimeters). They are seen best with MRI, but may also be seen on CT if the cysts are slightly larger. Pyelogenic cysts or calyceal diverticula are small cystic structures that connect with a portion of the pelvicalyceal system. On IVU, a calyceal diverticulum appears as a small round or oval collection of contrast connected to the fornix of the calyx. As stasis occurs within the diverticulum, renal stone formation may occur.

Para- and peripelvic cysts are extraparenchymal cysts that occur in the region of the renal pelvis. They may be single or multiple, unilateral or bilateral. With the increased use of cross-sectional imaging techniques, they are seen with increased frequency. They may result from lymphangiectasia from prior insult to the kidney. Depending on the size and number, IVU reveals compression of the renal pelvis and infundibula, but no calyceal dilatation. The condition may be confused with renal sinus lipomatosis. Ultrasound, CT, and MRI reveal the true nature of the process with the water-filled cystic structures in the renal sinus ( Fig. 27-60 ).



FIGURE 27-60  Peripelvic cysts—CT scan. Axial nephrographic phase (A) and excretory phase (B) images with a coronal excretory phase (C) image. Multiple bilateral water density cysts fill the renal hilum displacing and splaying the collecting system and renal pelvis (B, C). The cortex is preserved with no cysts visible in the cortex.



All imaging modalities have been used to discover renal masses. The distinction between solid and cystic lesions is paramount as it guides differential diagnosis and subsequent treatment as needed. As discussed previously, these are significant limitations with both IVU and US in discovering renal masses less than 2 cm to 3 cm in size.[179] The IVU also is very limited in differentiating cystic from solid lesions and should not be used for that purpose. Although less accurate than CT, US provides a noninvasive means for differentiating solid from cystic renal masses. If all imaging criteria for a renal cyst are met with US, an accurate diagnosis can be made. CT is the imaging modality of choice for the characterization of all solid mass, suspected solid masses, or masses that do not meet US criteria for a true renal cyst. [195] [196] [197] The advantage of CT lies in the multiphase manner in which studies can be performed. Noncontrast, arterial, corticomedullary, nephrographic, and excretory phase imaging may all play a role in the accurate display and characterization of renal masses. MRI has sensitivities and specificities in line with CT but is generally reserved for a case in which the patient has impaired renal function or a contraindication to iodinated contrast medium. It is technically more demanding but may be helpful in cases of indeterminate CT assessed renal masses, those with venous involvement, and in distinguishing vessels from retroperitoneal lymph nodes. The findings of any and all studies must be linked to the clinical history, especially in the case of complex or complicated cystic renal masses.

Renal neoplasms may arise from either the renal parenchyma or the urotheliem of the pelvicalyceal system. Renal tumors have been reported during every decade of life, including the newborn.[198] Both benign and malignant tumors occur within the kidney. Benign tumors of any significant size are extremely uncommon. The diagnosis is typically made at autopsy as they rarely cause symptoms. With the increased use of cross-sectional imaging techniques, more are being discovered. The renal adenoma is the most common benign neoplasm. Arising from mature renal tubular cells, it almost always is less than 2 cm to 3 cm in size. There are no characteristic radiologic features that distinguish it from often solid tumors. Typically these lesions will be corticomedullary in location, solid on US, and demonstrate uniform enhancement on CT. Other benign lesions have been reported including hamartomas, oncocytomas, fibromas, myomas, lipomas, and hemangiomas, but uncommonly.

Hamartomas of the kidney, angiomyolipomas (AML), are one group of benign renal tumors that are distinguishable radiologically.[199] As the AML is composed of different tissues, including fat, muscle, vascular elements, and even cartilage, the fat in particular may be detected radiographically.[200] AML occur in two different groups of patients. A solitary unilateral form is most frequently found in women from the third to fifth decade. These are usually discovered due to pain associated with hemorrhage. Multiple bilateral AMLs are found in patients with tuberous sclerosis. With marked involvement of the kidneys, there are multiple masses found bilaterally with an appearance not unlike that of polycystic disease, except for the presence of fat in the masses. The solitary AML may be seen as a renal mass on conventional studies, KUB, and IVU, if of sufficient size. US will demonstrate the mass to be solid with increased echoes due to the presence of fat in the lesion. [201] [202] CT is diagnostic in that fat will be seen with the mass ( Fig. 27-61 ). Usually the CT numbers will be -20 or less. Most AML have a large amount of fat and the diagnosis can be made with ease. Uncommonly only a minimal amount of fat is present, and it must be searched for diligently on thin-section noncontrast CT scans. [203] [204] All solid lesions in the kidney should be searched for fat; if it is present the diagnosis of AML is virtually assured. [205] [206] [207] Most AML 4 cm or less will be watched with surgery reserved for those of larger size, especially with hemorrhage. [208] [209] Oncocytoma is another benign renal tumor that may occasionally be suggested pre-operatively in a patient with a solid renal mass.[210] This uncommon benign tumor originates in the epithelium of the proximal collecting tubule. Radiologically, it is usually found incidentally in asymptomatic adults. Its features include a solid mass with homogenous enhancement, a central stellate scar that may be seen with US, CT, or MRI, and on angiographic spoked wheel pattern. [211] [212] [213] These findings are nonspecific, however, and histologic confirmation is needed. [214] [215] Oncocytic renal cell carcinomas also occur and surgery is generally needed for the correct diagnosis.



FIGURE 27-61  Angiomyolipoma—CT scan. Axial CT images—noncontrast (A), corticomedullary phase (B), nephrographic phase (C), and excretory phase (D). The fat-containing mass is seen projecting anteriorly from the left kidney. It has internal structure that demonstrates enhancement in this very vascular benign tumor.



Renal cell carcinoma is the third most common tumor of the genitourinary tract after carcinoma of the prostate and bladder. This tumor constitutes 2% to 3% of all adult tumors and is the most common retroperitoneal tumor. Clear cell renal carcinoma is the most common subtype accounting for 70% of cases. Its average 5-year survival is 55% to 60%. Papillary renal carcinoma represents 15% to 20% of cases with a 5-year survival of 80% to 90%; 6% to 11% of renal cell carcinomas are of the chromophobe subtype with a 5-year survival of 90%. Collecting duct renal cell carcinomas are the rarest with 1% of cases and a 5-year survival of less than 5%. Chromophobe and papillary tumors tend to grow slower, are less aggressive, and more likely to contain calcification within. [216] [217] [218]

Imaging studies in renal cell carcinoma are used for initial detection, characterization, and staging. Accurate staging is imperative as it drives the treatment decision. Surgery is the primary means of treatment with radical nephrectory, simple nephrectory, or nephron-sparing partial nephrectory being options. [219] [220] More recently radiofrequency ablation or cryoablation have been used successfully in a limited population. [221] [222] [223] Recently, immunotherapy for metastatic renal cell carcinoma has been delivered by CT guidance.[224]

The classic presentation of a renal cell carcinoma in a patient with painless hematuria is that of a renal mass. [50] [58] The plain film may reveal an enlarged kidney or mass in the region of the kidney; 10% to 20% of cases may demonstrate calcification on the KUB. Calcification may be seen however, in benign and malignant renal masses. Peripheral rim-like calcification on plain film does not exclude malignancy. Most often malignant lesions have central, punctuate, or mottled calcification.

Until recently the IVU has been the standard examination performed in patients suspected of having a mass lesion in the kidney.[179] Renal cell carcinoma will distort the kidney outline or cause renal enlargement.[50] The mass will have an irregular or indistinct junction with the normal renal parenchyma. The calyces will be stretched, distorted, or obliterated by the tumor. When the neoplasm extends medially into the renal pelvis, it will narrow or obliterate the renal pelvis or cause an irregular filling defect that represents either tumor or blood clot within the pelvis. A nonfunctioning kidney may be seen with renal vein occlusion, replacement of the majority of the kidney by tumor, or complete involvement of the renal pelvis. A mass lesion in the kidney requires further evaluation with cross-sectional imaging techniques. The US findings in a renal cell carcinoma include a mass with variable complex internal echoes, impaired through transmission and poor definition of the back wall or distal aspect of the lesion ( Fig. 27-62 ). Mural nodules may be seen in cystic lesions and the internal wall may be thickened and irregular. US is less accurate than CT for revealing small renal masses. Normal findings on US do not exclude a small renal mass. In one study of 205 lesions seen on CT, 79 were missed with US.[225] Thirty of these lesions were solid renal masses. Power Doppler US, phase-inversion tissue harmonic imaging, and US contrast-enhanced harmonic imaging may improve the sensitivity of US for the detection and characterization of solid renal masses. [226] [227] [228] [229]



FIGURE 27-62  Renal cell carcinoma—ultrasound. Longitudinal image reveals a solid mass projecting from the left kidney. The mass contains internal echoes and does not have any of the features of a renal cyst. It has an ill-defined interface with the kidney and no increased through transmission.



Computed tomography is the modality of choice for imaging renal cell carcinoma as it has been proven effective in detection, diagnosis, characterization, and staging with accuracy exceeding 90%. [219] [230] On noncontrast CT scans, renal cell carcinomas appear as an ill-defined, irregular area in the kidney with CT numbers close to that of renal parenchyma ( Fig. 27-63 ). After the injection of intravenous iodinated contrast, the vast majority of RCC will show significant enhancement. The best phase for depiction of the mass is the nephrographic phase, although lesions are certainly detectable on the corticomedullary and excretory phases as well (figs. 27-63 and 27-64 [63] [64]).[231] [232] [233] In the corticomedullary phase, there is maximal enhancement of the arteries and veins that must be seen for accurate staging and preoperative planning (see Fig. 27-64 ). [234] [235] The excretory phase is most helpful for showing the relationship of the RCC to the pelvicalyceal system and in preoperative planning for nephron-sparing partial nephrectomy (see Fig. 27-63 ). [236] [237] Clear cell RCC will tend to have greater enhancement than the papillary or chromophobe RCC (see figs. 27-63 and 27-64 [63] [64]). [238] [239] Enhancement patterns for clear cell and papillary RCC will appear more heterogeneous with the chromophobe RCC frequently showing a homogeneous enhancement pattern (see Fig. 27-63 ).[238] Chromophobe and papillary types will more often contain calcification than the clear cell type.[240]



FIGURE 27-63  Renal cell carcinoma—CT scan. Axial noncontrast (A), nephrographic phase (B), and excretory phase (C) images combined with a coronal nephrographic phase image. On the noncontrast scan (A) the right renal mass is slightly hyperdense relative to the rest of the kidney. Contrast-enhanced scans (B, C, D) show the enhancing surrounded by the normal renal parenchyma. This proved to be a renal cell carcinoma—chromophobe type.





FIGURE 27-64  Renal cell carcinoma—CT scan. Axial contrast-enhanced corticomedullary phase image. Note the heterogeneously enhancing mass in the anterior aspect of the left kidney. This is a stage II RCC as it has extended through the renal capsule into Gerota's fascia. This proved to be a renal cell carcinoma—clear cell type.



The staging of RCC is important in predicting survival rates and planning the proper surgical approach to the mass. Both the WHO and Robson classifications are used in the staging of renal cell carcinoma.[219] With the Robson classification, in a stage I RCC, the tumor is confined to the renal parenchyma by the renal capsule (see Fig. 27-63 ). In stage II RCC, there is tumor extension through the renal capsule into the perinephric fat but still within Gerota's fascia (see Fig. 27-64 ). Stage III lesions are subdivided as IIIa—tumor extension into the renal vein or IVC; IIIb—tumor involvement of regional retroperitoneal lymph nodes; and IIIc—tumor involving the veins and nodes ( Fig. 27-65 ). Stage IVa RCC will have progression of tumor outside Gerota's fascia with involvement of adjacent organs or muscles other than the ipsilateral adrenal gland. Stage IVb RCC represents tumor with distant metastases, the most common sites being the lungs, mediastinum, liver, and bone.



FIGURE 27-65  Renal cell carcinoma—CT scan. Coronal contrast-enhanced (A), axial contrast-enhanced (B), and coronal contrast-enhanced (C) images. Stage IIIA RCC with mass in the right kidney shows a tumor thrombus extending into the right renal vein. In a different patient the right renal mass also has a tumor thrombus, but it has extended into the inferior vena cava (B, C). Both these RCCs proved to be of the clear cell type.



Although RCC is the most common primary malignancy in the kidney, transitional cell carcinoma (TCC) also occurs within the kidney.[241] Most TCC involve the urothelium and project into the lumen of the renal pelvis or ureter. This leads to a picture of a filling defect within the renal pelvis or ureter that can be confused with a renal stone, blood clot, or debris ( Fig. 27-66 ). Transitional cell carcinoma of the bladder is much more common than TCC of the kidney or ureter.[242] The neoplasm may extend into the renal parenchyma and appears as a mass within the kidney. The imaging findings are similar to that of RCC except the lesions do not tend to enhance as much with contrast injection. Renal vein involvement is rare. Retrograde pyelograms with ureteroscopy are diagnostic.



FIGURE 27-66  Transitional cell carcinoma—IVU. The irregular filling defect in the left renal pelvis represents a TCC. Note that there is no significant obstruction of the left kidney with normal appearing calyces.



Lymphoma may involve the kidney as part of multi-organ involvement, or rarely as a primary neoplasm.[243] Lymphoma presents with single or multiple masses within one or both kidneys. Perirenal extension may be seen as well. An infiltrative picture may also be seen with lymphomatous replacement of the kidney. This form usually has adjacent retroperitoneal adenopathy. The imaging findings will be representative of either the mass or infiltrative involvement. CT has usually been the imaging method of choice in these patients. Metastatic disease may also involve the kidney. Actually, it is quite often found at autopsy. With individuals living longer with cancer and the development of new drugs, we will probably see a rise in the number of cases of visible renal metastases. Metastases are most commonly hematogenous and result in usually multiple foci of involvement, although single lesions do occur ( Fig. 27-67 ). They are most frequently seen with CT scanning, as CT is used for the regular follow-up of most cancer patients. Hypodense round masses usually in the periphery are the typical finding. When present as a single lesion, a metastasis cannot be differentiated from a primary renal neoplasm without biopsy.



FIGURE 27-67  Metastases to the kidney—CT scan. Contrast-enhanced nephrographic phase axial (A) and coronal (B) images. Multiple heterogeneous, but hypodense lesions are seen in the kidneys bilaterally with the largest in the left upper pole. These appeared in a 2-month period in a patient with metastatic lung carcinoma. Note the metastases also present in the liver.



Cystic renal masses present a vexing problem in that they are not all benign.[244] Cystic renal cell carcinomas occur, as do tumors within the wall of benign cysts. In 1986, Bosniak developed a classification system for cystic masses that has stood the test of time. [196] [245] [246] It is not a pathologic classification system, but actually an imaging and clinical management guide for handling the cystic renal mass. Category 1 represents simple benign cyst (see Fig. 27-58 ). Category 2 cysts are benign with thin septa, fine rim-like calcification, and/or uniform high-density cysts less than 3 cm that do not enhance with IV contrast injection on CT ( Fig. 27-68 ). Category 2F was added to deal with a group of lesions falling between category 2 and 3 that need follow-up, usually at 6 to 12 months, to prove benignity ( Fig. 27-69 ).[247] These cystic lesions may have multiple septa, an area of thick or nodular calcification, or a high-density cyst greater than 3 cm. Category 3 cystic lesions have thickened, irregular walls, which demonstrate some enhancement with contrast injection. Dense irregular calcification may also be seen. In these cases, clinical history may be helpful in pointing toward a renal abscess or infected cyst. Although many of these lesions will be benign, surgery may be necessary for diagnosis and treatment.[248] Biopsy has been advocated by some (see Fig. 27-52 ). [249] [250] [251] [252] Category 4 cystic masses are clearly malignant and demonstrate distinct enhancing soft tissue masses or nodules within the cyst ( Fig. 27-70 ). These lesions require nephrectomy, although if not larger than 5 cm to 6 cm and properly located, a nephron-sparing procedure may be performed.



FIGURE 27-68  Hyperdense renal cyst—CT scan. Axial noncontrast CT image. A single well-circumscribed hyperdense mass is seen in the right kidney. This represents a Bosniak type II renal cyst. It is sharply defined, less than 3 cm, and demonstrated no enhancement on the contrast-enhanced scan.





FIGURE 27-69  Bosniak type IIF renal cyst—CT scan. Axial nephrographic phase image. A cystic lesion in the right kidney also demonstrates large clumps of calcification on the outer wall and on internal septae. There was not change in the CT numbers between the noncontrast scan and the enhanced images. This requires follow-up. Note the Bosniak type I cysts in the left kidney.





FIGURE 27-70  Bosniak type IV renal cyst—CT scan. Coronal nephrographic phase image. The left kidney shows a cystic mass with an internal solid component in the lower pole. In the lower pole of the right kidney there is a solid mass with central necrosis with represents a RCC. Note the Bosniak type I cysts in the upper pole of the right kidney. There is also a renal calculus in the mid portion of the left kidney. The left lower pole cystic lesion proved to be a RCC—papillary type.



Cysts are well demonstrated on MRI due to excellent soft tissue contrast. On MR imaging, simple cysts are well circumscribed, thin-walled structures containing fluid that is dark on T1-weighted sequences and bright on T2-weighted sequences ( Fig. 27-71 ). Complex cysts are those that contain signal intensity material that is not characteristic for simple fluid. Complex cysts contain proteinaceous or hemorrhagic fluid and may have septations and calcification. The T1 signal intensity of the fluid is higher than expected for simple fluid, ranging from isointense to hyperintense. T2 signal intensity is lower than expected for simple fluid and may be black depending on the blood content. Cysts do not enhance. When compared to CT, MRI has been found to have a higher contrast resolution allowing for better visualization of septae. [253] [254] MRI also better characterizes blood products. MRI is more sensitive to subtle enhancement, especially with subtraction techniques, allowing MRI to surpass CT in differentiating a complex cyst from a cystic neoplasm [253] [254] [255] (figs. 27-72 and 27-73 [72] [73]). As with CT, MRI easily demonstrated the cysts of ADPK, AAPKD, and the cysts seen in hereditary disorders, such as chronic kidney injury ( Fig. 27-74 ), ADPCKD ( Fig. 27-75 ), and von Hippel-Lindau ( Fig. 27-76 ). MRI is a noninvasive way to confirm lithium toxicity by demonstrating characteristic parenchymal microcysts, in patients with chronic renal insufficiency who are on long-term lithium therapy.[256]



FIGURE 27-71  Simple cysts follow simple fluid signal intensity. A, On T2-weighted images cysts are bright and (B) on T1-weighted images cysts are dark. C, No enhancement is seen on gadolinium-enhanced T1-weighted images.





FIGURE 27-72  Complex cyst confirmed with image subtraction. A, T2-weighted axial image shows a bright left upper pole structure. B, T1-weighted axial image shows the same structure as intermediate in signal intensity. Because (C) post contrast T1 coronal shows higher signal intensity than expected for a cyst (arrow), (D) post contrast subtraction images are needed to confirm absence of enhancement (arrow).





FIGURE 27-73  Complex hemorrhagic cyst. A, T1-weighted axial images show a complex right renal structure, bright on both sequences and with internal septations. B, There is no enhancement on gadolinium-enhanced T1-weighted images. This was diagnosed as a hemorrhagic cyst with fine needle aspiration.





FIGURE 27-74  Chronic kidney injury. T2-weighted coronal image shows diffuse atrophy and multiple cysts in a patient on chronic dialysis.





FIGURE 27-75  Autosomal dominant polycystic kidney disease. A, Axial and (C) coronal T2-weighted images showing bilateral renal cortical atrophy and multiple cysts, most of which are bright. B, Axial T1-weighted images with multiple dark structures. These structures do not enhance after gadolinium injection, (D) and are therefore consistent with cysts.





FIGURE 27-76  Bilateral clear cell carcinoma in von Hippel-Lindau syndrome. Bilateral heterogeneous renal masses and left renal cyst seen on (A) T2- and (B) T1-weighted images (C) demonstrates heterogeneous enhancement of the larger right renal mass and more homogeneous enhancement of two smaller left renal masses. D, Maximum intensity projection presents the multiple renal masses in angiogram format.



Differentiating benign masses from malignant masses is not always possible. Oncocytomas and lipid poor angiomyolipomas may have similar characteristics to renal cell cancer. In most cases MRI characteristics are similar to CT and except for AML, most benign lesions cannot be distinguished from malignant lesions. Because angiomyolipomas contain macroscopic fat, MR imaging with fat suppressed and opposed-phase chemical shift sequences can be used to make an accurate diagnosis.[257] Signal intensity of fat is high on both T1- and T2-weighted sequences. Macroscopic fat in AML will drop in signal intensity with fat suppression sequences. Opposed-phase chemical shift sequences causes an “India ink” outline of the tumor at its interface with normal renal parenchyma. The enhancement pattern of AML is variable and depends on the composition of the lesion.

The MR appearance of renal cell carcinoma (RCC) can be variable because RCC is a neoplasm with many histologi-cal types. These include clear cell, which tend to be larger with associated hemorrhage and necrosis (figs. 27-77 and 27-78 [77] [78]), papillary ( Fig. 27-79 ), and chromophobe. RCC most commonly is heterogeneously hyperintense on T2-weighted sequences and hypointense to isointense on T1-weighted sequences ( Fig. 27-80 ). RCC enhances less than normal renal cortex and may be quite heterogeneous. The heterogeneity increases with increasing size due to variable amounts of necrosis and intraluminal lipid. The intra-luminal lipid may make areas of the mass drop in signal intensity on opposed phase T1-weighted sequences. Differentiating histological types is difficult due to overlap in their imaging appearance. The feasibility of RCC differentiation using advanced MR imaging techniques such as echoplanar is being evaluated but further research is required.[258]



FIGURE 27-77  Clear cell renal carcinoma, stage T3a. A, Axial T2-weighted image shows a 7.5 cm right renal mass with areas of high signal intensity, consistent with necrosis and cystic degeneration. B, Axial T1-weighted image showing a heterogeneous isointense mass with increased perinephric fat stranding. C and D, Axial and coronal gadolinium-enhanced images confirm central areas of necrosis. No venous invasion is seen. Focal microinvasion of the perinephric fat was seen at surgery.





FIGURE 27-78  Metastatic renal cell carcinoma, stage T4N2M1. A, Axial T2 and (B) gadolinium-enhanced T1-weighted images show a large heterogeneous mass with invasion of the adjacent liver and peritoneal metastases (arrowheads)C and D, Coronal gadolinium-enhanced T1-weighted images show the large mass extending inferiorly and medially, with invasion of the inferior vena cava to the level of the hepatic veins (arrowheads).





FIGURE 27-79  Papillary renal cell carcinoma, stage T1. Sagittal T1-weighted images (A) before and (B) after the administration of gadolinium show a subtle mass (arrow) in the anterior cortex and multiple nonenhancing cysts. No perinephric invasion was found at surgery.





FIGURE 27-80  Renal cell carcinoma with pseudocapsule, Stage 1. A, T2-weighted image shows a heterogeneous, bright mass on the left with a well-defined pseudocapsule. B, T1-weighted image confirms a well-defined dark mass involving the left renal cortex. C-E, Axial gadolinium-enhanced T1-weighted images in the arterial, venous, and excretory phases demonstrate heterogeneous enhancement and no evidence of renal vein involvement. No perinephric invasion was found at surgery.



Although MRI has been found to be highly accurate in staging RCC, the areas of greatest challenge remain the evaluation for local invasion of the perinephric fat and direct invasion of adjacent organs, especially with large tumors.[259] Presence of an intact pseudocapsule aids in excluding local invasion. A pseudocapsule is a hypointense rim around the tumor seen best on T2-weighted images (see Fig. 27-80 ). These are most frequently seen in association with small or slow-growing tumors. When the tumor extends beyond the confines of the kidney, the pseudocapsule is made of fibrous tissue, otherwise it is made up of compressed normal renal tissue.[260] If the pseudocapsule is intact, invasion of the perinephric fat is unlikely.[260]

Detecting and assessing vascular thrombosis in patients with RCC is highly accurate and reliable with contrast-enhanced MR imaging. [259] [261] Coronal imaging in the venous and delayed phases demonstrates the presence or absence of venous invasion, determines the extent of venous invasion, if present, and differentiates tumor thrombus, which enhances, from nonenhancing bland thrombus ( Fig. 27-81 ). Accurate determination of renal vein, inferior vena cava, and right atrial involvement is important for deciding the surgical approach.[262]



FIGURE 27-81  Poorly differentiated renal cell carcinoma, T4N2. A and B, Coronal and axial T2-weighted images show a heterogeneous mass in the lower pole of the left kidney with infiltration of the perinephric fat and extensive retroperitoneal lymphadenopathy. C, T1-weighted image shows the masses to be intermediate in signal intensity. D and E, axial gadolinium-enhanced T1-weighted images make the local invasion and adenopathy more conspicuous and show that the left renal vein is encased, not invaded (arrows).



Because findings of lymphoma are similar to CT, MRI likely will show no additional findings that would affect patient treatment. Lymphoma is typically hypointense on T1-weighted sequences and heterogeneous to slightly hypointense on T2-weighted sequences. Enhancement is minimal on post contrast sequences[263] ( Fig. 27-82 ). Vessels are usually encased, are not invaded, and necrosis is usually not seen. Treated lymphoma may vary in signal intensity, likely secondary to effects of therapy.[263]



FIGURE 27-82  Lymphoma. A, Coronal T2-weighted image shows a large, infiltrating left renal mass extending into the perirenal fat. B, Coronal gadolinium-enhanced T1-weighted image better delineates the mass from the renal cortex. C, Axial gadolinium-enhanced T1-weighted image shows encasement of the left renal vein (arrows).



Computed tomography urography and MR urography likely will show similar findings. TCC in the upper collecting system can either be a focal, irregular enhancing mass within the collecting system ( Fig. 27-83 ) or an ill-defined mass infiltrating the renal parenchyma. When small, they may be difficult to identify on both CT and MRI. Evaluation of the entire collecting system is required because synchronous lesions may be present. MRU is valuable for complete evaluation of the collecting system.



FIGURE 27-83  Transitional cell carcinoma. (A) Axial and (B) coronal T2-weighted images showing intermediate signal intensity masses (arrow) within the right renal pelvis associated with mild hydronephrosis. C and D, Axial gadolinium-enhanced T1-weighted images show heterogeneous enhancement and no evidence of invasion of the renal parenchyma.




Renal cell carcinoma (RCC) arises from the renal tubular epithelium and accounts for the majority of the adult kidney tumors. The tumor is angioinvasive and is associated with widespread hematogenous and lymphatic metastases especially to the lung, liver, lymph nodes, bone, and brain. Metastases are present in about 50% of patients at initial presentation. Radical nephrectomy is the main treatment for the early stages of disease, although palliative nephrectomy may also be performed in advanced disease with intractable bleeding. Solitary metastasis may also be resected. RCC responds poorly to chemotherapy. Radiation therapy for RCC is used for palliation of metastatic sites, specifically, bone and brain. Immunotherapy with biologic response modifiers such as interleukin-2 and interferon-α has the most impact on the treatment of metastatic disease. The 5-year survival may be as high as 80% to 90% for early stages of disease whereas advanced disease carries a poor prognosis.[264]

Preliminary studies of PET imaging of RCC have revealed a promising role in the evaluation of indeterminate renal masses, in preoperative staging and assessment of tumor burden, in detection of osseous and non-osseous metastases, in restaging after therapy, and in the determination of effect of imaging findings on clinical management. [265] [266] [267] [268] [269] [270] However, other PET studies have demonstrated less enthusiastic results and no advantage over standard imaging methods. [271] [272] [273]

A relatively high false-negative rate of 23% has been reported with FDG PET in the preoperative staging of RCC when compared with histological analysis of surgical specimens. In one recent study, PET exhibited a sensitivity of 60% (versus 91.7% for CT) and specificity of 100% (versus 100% for CT) for primary RCC tumors. For retroperitoneal lymph node metastases and/or renal bed recurrence, PET was 75.0% sensitive (versus 92.6% for CT) and 100.0% specific (versus 98.1% for CT). PET had a sensitivity of 75.0% (versus 91.1% for chest CT) and a specificity of 97.1% (versus 73.1% for chest CT) for metastases to the lung parenchyma. PET had a sensitivity of 77.3% and specificity of 100.0% for bone metastases, compared with 93.8% and 87.2% for combined CT and bone scan.[274] For re-staging RCC, a sensitivity of 87% and a specificity of 100% have been reported.[275] A comparative investigation of bone scan and FDG PET for detecting osseous metastases in RCC revealed sensitivity and specificity of 77.5% and 59.6% for bone scan and 100% and 100% for PET, respectively.[270] Another report revealed a negative predictive value of 33% and positive predictive value of 94% for restaging RCC.[266] Other studies have reported high accuracy in characterizing indeterminate renal masses with a mean tumor-to-kidney uptake ratio of 3.0 for malignancy.[265]

These mixed observations are probably related to the heterogeneous expression of glucose transporter-1 (GLUT-1) in RCC, which may not correlate with the tumor grade or extent. [276] [277] A negative study may not exclude disease whereas a positive study is highly suspicious for malignancy. If the tumor is FDG avid, then PET can be a reasonable imaging modality for follow-up after treatment and for surveillance ( Fig. 27-84 ). In fact, it has been shown that FDG PET can alter clinical management in up to 40% of patients with suspicious locally recurrent and metastatic renal cancer.[268]



FIGURE 27-84  Renal cell carcinoma. CT shows a large necrotic renal mass (A) with several bilateral pulmonary nodules (B). The PET scan (C) shows hypermetabolism at the periphery of the large renal mass and within the pulmonary nodules. The interior hypometabolism of the renal mass is compatible with central tumor necrosis.



The diagnostic accuracy of FDG PET appears not to be improved by semi-quantitative image analysis, which is probably due to the fundamental variability of glucometabolism in RCC.[273] In one study, the maximum and average standardized uptake values (SUVs) for FDG-positive primary renal malignant tumors were 7.9 +/- 4.9 and 6.0 +/- 3.6, respectively. The maximum and average SUVs of metastatic renal masses were 6.1 +/- 3.4 and 4.7 +/- 2.8, respectively. There was no significant difference in maximum and average SUVs between primary and metastatic renal masses.[278] Because FDG is excreted in the urine, the intense urine activity may confound lesion detection in and near the renal bed. Intravenous administration of furosemide has been proposed to improve urine clearance from the renal collecting system although the exact benefit of such intervention in improving lesion detection remains undefined.

Other PET tracers (e.g., 11C-acetate, 18F-fluoromisonidazole) have been investigated in the imaging evaluation of patients with RCC but further studies are needed to establish the exact role of these and other non-FDG tracers in this clinical setting. [279] [280] Moreover, many studies have now reported on the diagnostic synergism of the combined PET-CT imaging systems. The role of PET-CT in renal cancer imaging and its impact on both the short-term and the long-term clinical management and decision making will also need to be investigated.


Renal artery stenosis is a potential treatable cause of hypertension but is found in less than 5% of the hypertensive population.[281] When the expected signs and symptoms are present, the diagnosis may be made in 20% to 30% of patients.[282] RAS is usually defined as 50% or greater stenosis of the renal artery.[283] Atherosclerosis is the most common cause accounting for up to 70% of cases and is typically found in males over 50 years of age. The stenosis is caused by an atherosclerotic plaque with or without calcification located in the proximal renal artery at or near the ostia ( Fig. 27-85 ).[284] It is bilateral in 30% of cases. Fibromuscular dysplasia is the second most common cause—approximately 25%.[285] Fibromuscular dysplasia is sub-classified by the location of the involvement within the vessel wall with medial fibroplasia being the most common. This form has the classic findings of the string of beads in the distal main renal artery and segmental branches caused by the alternating areas of stenosis and dilatation.



FIGURE 27-85  Renal artery stenosis—CT angiogram. Axial CT image with vessel analysis. The origin of the left renal artery is markedly narrowed by calcified and non-calcified atherosclerotic plaque. The vessel analysis demonstrates the renal artery in cross section for accurate calculation of the degree of stenosis—greater than 70% in this case.



The IVU is of only historical note in the assessment of patients with renovascular hypertension. The hypertensive IVU was performed by obtaining a series of radiographs of the kidneys after the injection of contrast at 1-minute intervals looking for discrepancies in renal size, appearance of the nephrogram, prolongation of the nephrogram, and excretion patterns. This study is no longer performed because it has been supplanted by Doppler US, CT and MRI angiography, and captopril renography. [286] [287]

Conventional US and Doppler US have been used to assess patients with renovascular hypertension.[288] Renal size and the presence or absence of medical renal disease may be evaluated with grey-scale ultrasound. Doppler ultrasound has been employed to assess the main renal arteries for renal artery stenosis and the intrarenal vasculature for secondary effects with variable success. [289] [290] Doppler ultrasound is highly operator dependent and may be inadequate or incomplete due to overlying bowel gas, body habitus, or aortic pulsatility.[289] A stable Doppler signal may be difficult to reproduce in some patients. A complete examination has been possible in 50% to 90% of patients. Accessory renal arteries, which occur in 15% to 20% of patients may not be imaged.[291] The criteria used for evaluation of the main renal artery include an increase in the peak systolic velocity to greater than 185 cm/sec, a renal to aortic ratio of peak systolic velocity of greater than 3.0, and turbulent flow beyond the region of the stenosis.[292] Visualization of the main renal artery with no detectable Doppler signal would suggest renal artery occlusion. Intrarenal Doppler ultrasound vascular assessment has looked at the shape and character of the waveform. A dampened appearance to the waveform with a slowed systolic upstroke and delay to peak velocity, tardus-parvus effect, has shown variable results in renal artery stenosis.[293] A difference in the resistive indices of greater than 5% between the kidneys has also been suggestive of renal artery stenosis. Sensitivity and specificity for the techniques have generally been in the 50% to 70% range. Contrast-enhanced ultrasound has been suggested as a means to improve the accuracy of Doppler ultrasound. [294] [295]

Computed tomography angiography performed with a multidetector CT (MDCT) scanner has sensitivity and specificity at or near 100% (see Fig. 27-85 ). [296] [297] [298] A normal result should rule out renal artery stenosis.[299] This study is performed with a contrast injection of 4 to 5 cc/sec, volume of contrast of 100 to 120 cc, and rapid scanning at 15 to 20 seconds for proper assessment of the renal arteries. The angiographic study takes less than 10 seconds to complete.[296] Computer processing of images is imperative with 3D volume renderings and maximum intensity projection (MIP) images required (figs. 27-86 and 27-87 [86] [87]). [299] [300] [301] Assessment of the axial images alone is insufficient. The main renal artery as well as its segmental braches can be viewed and evaluated. Accessory renal arteries down to 1 mm in diameter can be seen.[302] CTA may also demonstrate other findings in the patient with RAS including a smaller kidney with a smooth contour, thinning of the cortex, a delayed or prolonged nephrogram—all on the affected side. Patients with renal artery stents can be successfully imaged with CTA ( Fig. 27-88 ).[303] [304] CTA and MRA are equivalent in the detection of hemodynamically significant renal artery stenosis.[305] Patients with impaired renal function or contrast allergy will need evaluation with MRA as a CTA with iodinated contrast cannot be done. Digital subtraction angiography should be reserved for those patients requiring an intervention, either angioplasty or angioplasty and stent placement. It is unnecessary for diagnosis today.



FIGURE 27-86  Renal artery stenosis—CT angiogram. Image processing applied to case in Figure 27-53 . Axial (A) and coronal (B) slab MIP images demonstrate the atherosclerotic stenosis of the proximal renal artery. Note the accessory renal artery arising adjacent to the left main renal artery. Volume rendering of the CT angiogram (C) results in this 3D display, which may be rotated for best viewing and analysis.





FIGURE 27-87  Renal artery stenosis—CT angiogram. Image progressing of abdominal CT angiogram. Coronal slab MIP (A) demonstrates the smooth narrowing of the proximal right renal artery in this patient with Takayasu arteritis. Note the markedly abnormal aorta with occlusion distal to the origin of the renal artery. Volume rendering (B) of the CT angiogram with vessel analysis reveals the 80% stenosis of the right renal artery. The left renal artery had been occluded previously and the kidney was supplied by collateral vessels.





FIGURE 27-88  Renal artery stent—CT scan. Axial (A) and coronal (B) images of a contrast-enhanced CT scan in the corticomedullary phase. The metallic stent is seen at the origin of the right renal artery. It had been placed for treatment of renal artery stenosis due to atherosclerosis. Good flow through the stent is seen as contrast fills the lumen.



Ultrasound, CTA, and MRA have been shown to be accurate alternatives to conventional angiography. [306] [307] Because CTA is sensitive, accurate, fast, and reproducible, MRA is reserved for patients for whom iodinated contrast is contraindicated. Renal insufficiency is not uncommon in the population clinically selected for high risk of renal artery stenosis. For this reason CE-MRA is widely accepted as a reliable and accurate examination for the evaluation of renal artery stenosis in this patient group. [88] [305] [308] [309] Like CTA, MRA is noninvasive and provides excellent visualization of the aortoiliac and renal arteries.[305]

Contrast-enhanced-MRA has over 95% sensitivity for demonstrating the main renal arteries and has a high negative predictive value. A normal CE-MRA almost completely excludes a stenosis in the visualized vessels.[307] CE-MRA is a reliable examination but has been limited by incomplete visualization of segmental and small accessory vessels.[310] Whereas visualization of all accessory vessels is desired, Bude and colleagues[311] found isolated hemodynamically significant stenosis of an accessory artery in only 1.5% of their patients (1 of 68). The authors concluded that this limitation does not substantially reduce the rate of detection of renovascular hypertension by MRI. With the use of 3D reconstruction, studies have demonstrated no significant difference between CE-MRA and multidetector CTA in the detection of hemodynamically significant renal artery stenosis.[305] Volume rendering and multiplanar reformatting improve accuracy in depicting renal artery stenosis.[87] Volume rendering increases the positive predictive value of CE-MRA by reducing the overestimation of stenosis found with earlier reconstruction techniques ( Fig. 27-89 ). [88] [307] Volume rendering has better correlation with digital subtraction angiography and improves delineation of the renal arteries.[88]



FIGURE 27-89  Renal artery stenosis. Advancements in post processing allow for more accurate evaluation of stenosis with MR angiography. A, Maximum intensity projection shows a high-grade stenosis near the renal artery origin with areas of apparent narrowing in the mid renal artery (arrowheads), mimicking fibromuscular dysplasia. B, Volume image show the proximal stenosis (arrowhead), but the mid artery is more normal in appearance. C, Image showing the artery in 2D allows measurement of the proximal stenosis and demonstrated a normal mid artery. This stenosis was confirmed with angiography.



Limitations of MRA are due in part to limitations in resolution and motion artifacts. [306] [312] Advancements in MR gradient strengths and newer MRA techniques are resulting in continued improvement in image resolution and reduction in motion artifacts, while reducing imaging times.[312] Work with cardiac imaging has demonstrated that imaging at 3T can result in higher spatial and temporal resolution, when compared with imaging at 1.5T. This higher resolution was found to improve the evaluation of smaller structures of the heart.[313] Further evaluation is needed to determine how imaging at 3T will affect MRA of the renal arteries.[314]

Phase contrast MRA can be used to calculate blood flow through the renal artery.[315] Phase contrast flow curves can be generated and the severity of the hemodynamic abnormalities can be graded as normal, low-grade, moderate, and high-grade stenosis. This is similar to the Doppler ultrasound method. Grading can be used to evaluate the hemodynamic significance of a detected stenosis.[316] The significance of a stenosis on parenchymal function, however, is not currently evaluated by conventional MRA. Initial renal MR imaging perfusion studies are being performed to grade the effect of renal artery stenosis on parenchymal perfusion. Initial results show that MRI perfusion measurements with high spatial and temporal resolution reflect renal function as measured with serum creatinine.[317] Volumetric analysis of functional renal cortical tissue may also give clinically useful information in patients with renal artery stenosis.[318] Further research is required before this will be known, however.

Magnetic resonance angiography is currently of limited value for the evaluation of restenosis in patients with renal artery stents. Although stent technology is rapidly changing, metal artifact still obscures the stent lumen to varying degrees due to susceptibility artifacts ( Fig. 27-90 ). Phase-contrast MRA may be used to measure velocities proximal and distal to the stent, but this is an indirect approach to evaluating for stenosis. Work is being done to develop a metallic renal artery MR imaging stent that will allow for lumen visualization; however, this is not currently available clinically.[319]



FIGURE 27-90  Magnetic resonance angiography in a patient with bilateral renal artery stents (arrowheads). The metal in the stent causes artifact that obscures the vessel lumen. Contrast is seen beyond the stent indicating that there is no complete occlusion.



Fibromuscular dysplasia (FMD) has a characteristic appearance of focal narrowing and dilatation (“string of beads”) ( Fig. 27-91 ). Because FMD frequently involves the mid to distal renal artery and segmental branches, resolution limits MRA evaluation. For this reason, MRA is not as reliable for diagnosis of FMD as it is for RAS. Renal infarctions are well demonstrated on MRA as wedge-shaped areas of decreased parenchymal enhancement. These are most conspicuous on the nephrographic phase. Evaluation of the arterial and venous structures may demonstrate the origin of the emboli or thrombosis ( Fig. 27-92 ).



FIGURE 27-91  A and B, MR angiography with volume reconstruction demonstrates a subtle irregularity in the mid right renal artery (arrow). Fibromuscular dysplasia was confirmed with conventional angiography.





FIGURE 27-92  Renal infarcts due to embolic disease. A, Coronal gadolinium-enhanced T1-weighted image shows wedge-shaped cortical areas of absent enhancement (arrowheads)B, Axial gadolinium-enhanced T1-weighted image shows an irregular filling defect in the aorta (large arrowhead) consistent with thrombus, and three focal defects in the spleen (small arrowheads) consistent with splenic infarcts.




Angiotensin converting enzyme (ACE) inhibition prevents conversion of angiotensin I to angiotensin II. In renal artery stenosis, angiotensin II constricts the efferent arterioles as a compensatory mechanism to maintain GFR despite diminished afferent renal blood flow. Therefore, ACE inhibition in renal artery stenosis reduces GFR by interfering with the compensatory mechanism. Captopril renography has been successful in evaluating patients with renal artery stenosis.

Before the study, the patient should be well hydrated. ACE inhibitors should be discontinued (captopril for 2 days; enalapril or lisinopril for 4 to 5 days) because otherwise diagnostic sensitivity may be reduced. Diuretics should be discontinued preferably for 1 week. Dehydration resulting from diuretics may potentiate the effect of captopril and contribute to hypotension. Captopril (25 mg to 50 mg) crushed and dissolved in 250 mL water is administered orally followed by blood pressure monitoring every 15 minutes for 1 hour. Alternatively, enalaprilat (40 mg/kg up to 2.5 mg) is administered intravenously over 3 to 5 minutes. A baseline scan can be performed before captopril renography (1-day protocol) or the next day, only if captopril study is abnormal (2-day protocol).

The affected kidney in renovascular hypertension (RVH) often has a renogram curve with reduced initial slope, a delayed time to peak activity, prolonged cortical retention, and a slow downslope following peak ( Fig. 27-93 ). These findings are due to slowed renal tracer transit owing to increased solute and water retention in response to ACE inhibition. Reduced urine flow causes delayed and decreased tracer washout into the collecting system in Tc-99m MAG3 and I-131 OIH studies. Tc-99m DTPA demonstrates reduced uptake on the affected side.[320]



FIGURE 27-93  Tc-99m MAG3 renograms before (A) and after (B) ACE inhibition with captopril. Note the relatively normal renograms in A and the reduced initial slope, delayed time to peak activity, and plateau compatible with captopril-induced cortical tracer retention in B. These findings suggest a high probability for hemodynamically significant bilateral renal artery stenosis that is more severe on the left side (connected squares) than the right side (connected diamonds). Bilateral renal artery stenosis was later confirmed with angiography.  (Adapted from Saremi F, Jadvar H, Siegel M: Pharmacologic interventions in nuclear radiology: Indications, imaging protocols, and clinical results. Radiographics 22:447–490, 2002.)




Consensus reports regarding methods and interpretation of ACE renography elaborate on a scoring system of renogram curves. [321] [322] [323] It has been recommended that high (>90%), intermediate (10% to 90%), and low (<10%) probability categories be applied to captopril renography based on change of renogram curve score between baseline and post-captopril renograms. Among quantitative measurements, relative renal function, the time to peak activity, and the ratio of 20-minute renal activity to peak activity (20/peak) are used more commonly than other parameters. For MAG3 renal scintigraphy, a 10% change in relative renal function, peak activity increase of 2 minutes or more, and a parenchymal increase in 20/peak post captopril by 0.15 represent a high probability of renovascular hypertension.[324]

Captopril renography has a sensitivity of 80% to 95% and a specificity of 50%; the detection of stenosis by captopril-stimulated renography may be more complicated.[320] It is more the exception than the rule for bilateral renovascular stenosis to have symmetric findings on captopril renography. Studies in canine model with bilateral renal artery stenosis demonstrated that captopril produced striking changes in the time-activity curve of each kidney, which are more pronounced in the more severely stenotic kidney.[320]


Renal vein thrombosis is usually clinically unsuspected. It is found in patients with a hypercoagulable state, underlying renal disease, or both.[325] The classic presentation of acute RVT with gross hematuria, flank pain, and decreasing renal function is uncommon.[326] Nephrotic syndrome is a common mode of presentation.[327] Two thirds of patient will present with minimal or no symptoms. In one study, 22% of patients with nephrotic syndrome were found to have RVT, usually chronic and asymptomatic; 60% of these patients had membranous glomemlonephritis.[327] Other etiologies include collagen vascular diseases, diabetic nephropathy, trauma, and tumor thrombus. Renal venography has been the definitive method of diagnosis in the past, but other methods of evaluation including Doppler US, CT, and MR have supplemented it.

The IVU is nonspecific in the diagnosis of RVT and is no longer employed. It may be normal in more than 25% of cases. With grey-scale and Doppler US the involved kidney appears enlarged and swollen with relative hypoechogenicity when compared with the normal size.[326] The finding of a filling defect in the renal vein is both sensitive and specific for diagnosis and is the only convincing sign of RVT. The lack of flow on Doppler US, however, is a nonspecific finding and is frequently due to a technically limited study. Absence or reversal of the diastolic waveform with Doppler US should not be used to suggest RVT.

A contrast-enhanced CT study is needed to properly assess the patient with suspected renal vein thrombosis. If there is renal function impairment MRI must be employed. CT findings include an enlarged renal vein with a low attenuating filling defect representing the clot within the renal vein.[328] There may be abnormal parenchymal enhancement with prolonged corticomedullary differentiation and a delay or persistent nephrogram. The kidney will appear to be enlarged with edema in the renal sinus. There may be stranding and thickening of Gerota's fascia. A striated nephrogram may occasionally be seen. Attenuation of the pelvicalyceal system may occur due to edema. Delayed appearance or absence of the pelvicalyceal system altogether may also be seen. Within chronic RVT, the RV may be attenuated or narrowed due to clot retraction and peri-capsular collateral veins may be noted. There is an increased risk of pulmonary emboli in these patients as well. With renal and rarely adrenal tumors, there may be thrombus that develops in the RV with extension to the IVC. Inhomogeneous enhancement of the thrombus suggests direct tumor involvement, not a bland thrombus.

The appearance of renal vein thrombosis on non contrast-enhanced MRI is variable. If the thrombosis is acute, the renal vein will be distended, no normal flow void is seen, and the affected kidney will be enlarged. Renal infarction may also be present. If the thrombosis is chronic, the renal vein will be small and difficult to see. The vein will contain a non-enhancing filling defect on contrast-enhanced MR venography consistent with thrombus. Enhancement of the thrombus is characteristic of tumor.


The treatment of choice for patients with end-stage renal disease is renal transplantation. Although there has been significant improvement in continuous peritoneal dialysis and hemodialysis, patient survival is longer and overall quality of life is better after renal transplantation. Radiological evaluation is performed on the renal transplant donor and in the post-operative assessment of the transplant recipient. Although IVU and angiography were used in the past, US, CT, MRI, and renal scintigraphy are the current methods employed in these patients ( Fig. 27-94 ). [329] [330] [331]



FIGURE 27-94  Normal renal transplant—ultrasound. Coronal image (A) of a recently transplanted kidney in the right lower quadrant. The central echo complex, medullary pyramids, and cortex are well seen. The duplex Doppler (B) image demonstrates normal flow to the transplant with a normal resistive index of 0.56.



A comprehensive radiological assessment of the living renal transplant donor is crucial.[332] The anatomic information that is necessary is vascular, parenchymal, and pelvocalyceal. The renal artery must be visualized for number, length, location, and branching pattern. The parenchyma must be evaluated for scars, overall volume, renal masses, and calculi. The venous anatomy must be seen and the number of veins, anatomic variants, and significant systemic tributaries noted. The pelvocalyceal system must be scrutinized for anomalies such as duplication and papillary necrosis. As a choice exists for the type of nephrectomy, laparoscopic or open, complete and accurate information is necessary. The limited field of view with laparoscopic nephrectomy requires this information for a safe procedure. [333] [334] [335] [336]

With the development of multidetector CT (MDCT) scanners, the complete evaluation of the living renal transplant donor is possible. [333] [337] [338] A non-contrast low-dose CT scan is performed just to search for renal stones, locate the kidneys, and identify renal masses (see Fig. 27-9 ). Arterial phase scanning is generally performed at 15 to 25 seconds to demonstrate the main renal artery, branching pattern of the artery, and abnormalities such as atherosclerotic plaques or fibromuscular dysplasia (see Fig. 27-11 ); 25% to 40% of patients have accessory renal arteries and 10% have early branching patterns in the main renal artery. [334] [336] The transplant surgeon requires a main renal artery free of branching for the first 15 mm to 20 mm. Due to the rapid transit of contrast through the kidney, most renal veins are well seen in this phase also (see Fig. 27-10 ). Venous variants occur in 15% to 28% of patients with multiple renal veins being most common, especially in the right. On the left side 8% to 15% have a circumaortic renal vein and 1% to 3% a retroaortic vein. [336] [339] Venous tributaries are also important to visualize including the gonadal, left adrenal, and lumbar veins. These are best seen on the nephrographic phase. [334] [335] This phase is performed at 80 to 120 seconds after injection and is used to evaluate the cortex and medulla for scars and masses (see Fig. 27-12 ). Excretory phase imaging is performed with a CT scan, CT digital radiograph, or plain films to note the pelvocalyceal system for anomalies or abnormalities (see figs. 27-13 and 27-14 [13] [14]). CT has demonstrated accuracy of 91% to 97% for arterial phase imaging, 93% to 100% for the venous phase, and 99% for the pelvocalyceal system. [338] [340] [341] Similar results have been noted for MRI with the biggest discrepancy being found in imaging accessory renal arteries. [342] [343] The lack of ionizing radiation and iodinated contrast will make MRI attractive in the future. Most centers today use CT in the evaluation of living renal transplant donors.

Magnetic resonance imaging, MRA, and MRU can be combined into one examination for the evaluation of the renal transplant donor.[344] MRI and CT are comparable for the evaluation of renal vasculature, morphology, and function. In order to avoid radiation exposure and nephrotoxicity, MRI may be chosen over CT for pre-operative evaluation.

Quantification of functional renal volume with MRA has been demonstrated to be feasible in healthy renal donors by determining the cortical volume.[345] The hypothesis supported by Van den Dool and colleagues was that glomerular filtration is an important component of renal function, and because the majority of glomeruli are in the cortex, there should be good correlation between renal function and cortical volume. Further research is required to confirm the authors' findings, however.

After surgically successful renal transplantation, radiological evaluation is frequently necessary. Conventional sonography, Doppler US, CT, MRI, and renal scintigraphy are used in various settings. Ultrasound assumes the primary role for assessing patients with changes in serum creatinine, urine output, pain, or hematuria.[346] It is also used to direct renal biopsy. Doppler US is used to evaluate renal perfusion, the patency of the renal artery and venous, and the integrity of the vascular anastomoses.[347] CT, MRI, and renal scintigraphy are adjunctive studies.

Conventional grey-scale ultrasound is essential to assess for transplant obstruction and peritransplant fluid collections.[331] Conventional sonography yields nonspecific findings in ATN and acute rejection including obliteration of the corticomedullary junction, prominent swollen pyramids, and loss of the renal sinus echoes. [330] [332] All these findings indicate edema of the transplant, which leads to increased peripheral vascular resistance, decreased diastolic perfusion, and elevation of the resistive index (>0.80) ( Fig. 27-95 ).[334] Chronic rejection may lead to a kidney with diffusely increased echogenicity throughout.



FIGURE 27-95  Renal transplant with ATN—ultrasound. Duplex Doppler image of the transplanted kidney shows a normal size and normal appearing kidney with a high resistive index of 0.80 in the interlobar artery. The patient recovered with return of normal renal function in 5 days.



Doppler US adds valuable information pertaining to the integrity of the vascular elements. Despite early enthusiasm with the ability of Doppler US to differentiate acute transplant rejection from acute tubular necrosis, it is now known that the findings are nonspecific and cannot obviate the need for renal biopsy in these cases.[348] Both ATN and acute rejection can cause increased peripheral vascular resistance. [349] [350] A significant number of patients with acute rejection have a normal resistive index (<0.80). It is now known that vascular rejection is no more likely to cause increased peripheral vascular resistance than cellular rejection.[348] Neither the timing nor clinical symptoms of the renal dysfunction can be used to differentiate acute rejection from ATN.[348] Doppler US is most helpful in detecting acute arterial thrombosis where there is an absent signal in the artery or renal vein thrombosis where there is a plateau-like waveform and retrograde diastolic flow. An abnormal Doppler waveform in the allograft indicates a compromised transplant.[351] Sequential examinations may be used to show improvement or deterioration in the condition affecting the kidney and to note the progress of treatment.

Magnetic resonance imaging is useful in patients where the transplant is obscured by overlying bowel gas or in patients with large body habitus where ultrasound may be limited by the depth of the transplant. MRI is favored over contrast-enhanced CT due to lower risk of renal parenchymal injury associated with gadolinium. If any doubt exists after a thorough ultrasound evaluation, MR imaging may be performed to clarify or confirm the ultrasound findings.

Peri-transplant fluid collections are very common, occurring in up to 50% of cases.[346] These fluid collections may represent urinoma, hematoma, lymphocele, abscess, or seroma. The impact of the collection depends on the size and location. Urinomas and hematomas are found early, usually immediately after surgery. Lymphoceles generally are not found until 3 to 6 weeks after surgery. Abscesses are usually associated with transplant infection. On US evaluation, extrarenal or subcapsular hematomas usually have a complex echogenic appearance, which becomes less echogenic with time ( Fig. 27-96 ).[346] CT will demonstrate a high attenuation fluid collection early. These are usually too complex to be drained successfully percutaneously. Urine leaks and the associated urinoma are also found in the immediate postoperative period ( Fig. 27-97 ).[346] US will show an anechoic fluid collection with no septations. They may rapidly increase in size. Drainage may be performed by either US or CT guidance.[352] Antegrade pyelography via a percutaneous nephrostomy is needed to detect the site of leak, usually the ureteral anastomoses. Stent placement for treatment is necessary. Lymphoceles are recognized weeks to years after transplantation and occur in up to 20% of cases.[346] They form from the leakage of lymph from the interrupted lymphatics at surgery. Lymphoceles appear as anechoic fluid collections on US with septations. The size and effect on the kidney determine the need for treatment. As they are frequently located medial and inferior to the kidney, they are a common cause of obstruction to the kidney. US or CT guidance for drainage may be used. Sclerotherapy may be needed in a minority of cases to treat the lymphocele.[352] Peri-transplant abscess usually develops in association with renal infection or the infection of other fluid collections in the immunocompromised patient. Abscess on US examination appears as a complex fluid collection, possibly containing gas.[346] Fluid aspiration is usually necessary for the accurate characterization of fluid within a collection. Because blood products have characteristic signal intensities on T1- and T2-weighted sequences, MRI can provide specific diagnostic information that may help avoid an unnecessary interventional procedure, in cases of hematoma.



FIGURE 27-96  Renal transplant with hematoma—ultrasound. Longitudinal image of the upper aspect of the transplanted kidney shows two hypoechoic collections adjacent to the kidney. The heterogeneous hypoechoic nature of the collections suggests that they represent hematomas as opposed to urinomas or lymphoceles, which generally would be anechoic.





FIGURE 27-97  Renal transplant with urinoma—ultrasound. Transverse image through the lower aspect of the transplanted kidney reveals a normal appearing kidney with a large anechoic fluid collection adjacent to it. This was aspirated under ultrasound guidance leading to the diagnosis of urinoma. The patient was treated with catheter placement and drainage also performed with ultrasound guidance.



Renal obstruction or hydronephrosis may be seen in the transplanted kidney with renal dysfunction and is reversible. US is the best means for assessment.[347] In the immediate post-transplant period, mild caliectasis is common due to edema at the ureteric anastomosis site. Obstruction may also be caused by peritransplant fluid collections that may be seen also with US. Blood clots within the pelvicalyceal system may also yield hydronephrosis. Later strictures may occur primarily at the ureteral anastomosis site. Renal stones may also cause hydronephrosis during their passage to the bladder. A functional obstruction may be seen with an over distended bladder. US will demonstrate a resolution of the hydronephrosis with bladder emptying.

Hypertension with or without renal dysfunction may be seen in many post-transplant patients.[346] Vascular and nonvascular causes must be differentiated. Doppler US is the first line of evaluation. Renal artery stenosis may be found in up to 23% of patients.[353] The stenosis may occur before the anastomosis in the iliac artery, at the anastomosis site or more distally. More than half of the cases have the stenosis at the anastomotic site with it being more common in end to end anastomosis. CT or MR angiography is used to determine the site and the degree of stenosis ( Fig. 27-98 ). Angioplasty is successful in managing most cases.[353]



FIGURE 27-98  Renal transplant MR angiography showing (A) normal arterial and (B) normal venous anastomoses.



Arteriovenous fistula occurs in transplant patients after renal biopsy. Most will close spontaneously within 4 to 6 weeks. Color and duplex Doppler imaging demonstrate high velocity and turbulent flow localized to a single segmental or interlobar artery and the adjacent vein. There is arterialized flow noted in the draining vein. Grey-scale images only demonstrate a simple or complex appearing cystic structure. If large and growing, embolization may become necessary.

Neoplasm occurs in transplant patients with increased frequency, up to 100 fold.[346] Neoplasms develop due to prolonged immunosuppression. Skin cancers and lymphoma are the most common. There may be an increased risk of renal cell carcinoma in the transplanted kidney. Post-transplantation lymphoproliferative disorder (PDLD) may occur in renal transplant patients.[354] Although the transplanted kidney may be involved, the most frequent sites are the brain, liver, lungs, and gastrointestinal tract. The appearance is similar to that found in conventional lymphomas with mass lesions in the organs with or without associated adenopathy.

The MRI findings of rejection are nonspecific (figs. 27-31, 27-32, and 27-99 [31] [32] [99]). More recently, Sadowski and colleagues demonstrated the feasibility of using blood oxygen level-dependent MR imaging to evaluate the renal transplant oxygen status and presence of acute rejection.[355] The authors conclude that MR imaging may differentiate acute rejection from normal function and acute tubular necrosis, but further research is required. Animal research is being performed with the hope of using noninvasive diffusion MR imaging techniques as a tool for monitoring early renal graft rejection after transplantation.[356]



FIGURE 27-99  Renal transplant graft with normal function. A, Axial T2-weighted; B, axial T1-weighted; and C, axial gadolinium-enhanced T1-weighted images.



Nuclear medicine procedures are also employed in the renal transplant patient and play a role in the assessment of the complications associated with transplantation. These include vascular compromise (arterial or venous thrombosis), lymphocele formation, urine extravasation, acute tubular necrosis, drug toxicity, and organ rejection. Scintigraphy provides important imaging information about these potential complications, which can then prompt corrective intervention.[357]

An earliest complication may be hyperacute rejection, which is often apparent immediately after transplantation and is due to preformed cytotoxic antibodies. Other early complications may include sudden urine output decline and acute urinary obstruction. Scintigraphy with DTPA or MAG3 shows absence of perfusion and function with complete renal artery or vein thrombosis. A sensitive but nonspecific finding for acute rejection occurs when there is greater than 20% decline in the ratio of renal activity to the aortic activity.[358]

Renal scintigraphy performed a few days after the transplantation often shows intact perfusion but delayed and decreased tracer excretion and some cortical tracer retention. This is typically due to acute tubular necrosis (ATN) and is more common with cadaveric grafts than with living-related grafts ( Fig. 27-100 ). If both perfusion and function continue to decline, then rejection should be considered. However, ATN, obstruction, drug (cyclosporine) toxicity, and rejection can have relatively similar scintigraphic appearance. The differential diagnosis should be considered in the clinical context and the interval since transplantation, although two or more of these conditions may coexist. In one report, a non-ascending second phase of MAG3 renogram curve was predictive of graft dysfunction. However, patients with ATN were not significantly more likely to have a non-ascending curve than those with acute rejection. An ascending curve was nonspecific and could be seen in both normally and poorly functioning grafts.[359]



FIGURE 27-100  Abnormal Tc-99m MAG3 renogram demonstrating pattern compatible with acute tubular necrosis involving the right pelvic living-related renal transplant.



Urine extravasation may be noted on the renal scans as collection of excreted radiotracer outside of the transplant and the urinary bladder. Small urine leaks and impaired renal transplant function make the identification of a leak difficult on scintigraphy. However, a cold defect that becomes warmer with time on the sequential images usually represents an urinoma or a urinary leak. If the activity declines with void-ing, then the finding is likely an urinoma. A chronic photopenic defect may represent a hematoma or a lymphocele (or both).[360] For assessing potential obstructive disease, scintigraphy with a diuretic may be considered as previously discussed.


1. Amis ES: Epitaph for the urogram (editorial).  Radiology  1999; 213:639-640.

2. Pollack HM, Banner MP: Current status of excretory urography: A premature epitaph?.  Urol Clin North Am  1985; 12(4):585-601.

3. Dyer RB, Chen MYM, Zagoria RF: Intravenous urography: Technique and interpretation.  RadioGraphics  2001; 21:799-824.

4. Hattery RR, Williamson Jr B, Hartman GW, et al: Intravenous urographic technique.  Radiology  1988; 167:593-599.

5. Saxton HM: Review article: Urography.  Br J Radiol  1969; 42:321-346.

6. Fry IK, Cattell WR: The nephrographic pattern during excretion urography.  Br Med Bull  1972; 28:227-232.

7. Katzberg RW: Urography into the 21st century: New contrast media, renal handling, imaging characteristics and nephrotoxicity.  Radiology  1997; 204:297-312.

8. Almer T: Contrast agent design: Some aspects of synthesis of water-soluble contrast agents of low osmolality.  J Theo Biol  1969; 24:216-226.

9. McClennan BL: Ionic and nonionic iodinated contrast media: Evolution and strategies for use.  Am J Roentgenol  1990; 155:225-233.

10. Lasser EC: Etiology of anaphylactorial responses: The promise of nonionics.  Invest Radiol  1985; 20:579-583.

11. Shehadi WH: Contrast media adverse reactions: Occurrence, recurrence, and distribution patterns.  Radiology  1982; 143:11-17.

12. Katayama H, Yamaguchi K, Kozuka T, et al: Adverse reactions to ionic and nonionic contrast media: A report from the Japanese Committee on the Safety of Contrast Media.  Radiology  1990; 175:621-628.

13. Jacobsson BF, Jorulf H, Kalantar MS, Narasimham DL: Nonionic versus ionic contrast media in intravenous urography: Clinical trial in 1000 consecutive patients.  Radiology  1988; 167(3):601-605.

14. Brasch RC: Allergic reactions to contrast media: Accumulated evidence.  Am J Roentgenol  1980; 134:797-801.

15. Lasser EC: Basic mechanisms of contrast media reactions: Theoretical and experimental considerations.  Radiology  1968; 91:63-65.

16. Lasser EC, Berry CC, Talner LB, et al: other Contrast Material Reaction Study participants: Pre-treatment with corticosteroids to alleviate reactions to intravenous contrast material.  N Engl J Med  1987; 317(14):845-849.

17. Taliercio CP, Vietstra RE, Fisher LD, Burnett JC: Risks of renal dysfunction with cardiac angiography.  Ann Intern Med  1986; 104:501-504.

18. Hou SS, Bushinsky DA, Wish JB, et al: Hospital-acquired renal insufficiency: A prospective study.  Am J Med  1983; 74:243-248.

19. Tublin ME, Murphy ME, Tessler FN: Current concepts in contrast media-induced nephropathy.  Am J Roentgenol  1998; 171:933-939.

20. Barrett BJ, Carlisle EJ: Metaanalysis of the relative nephrotoxicity of high-and low-osmolality iodinated contrast media.  Radiology  1993; 188:171-178.

21. Aspelin P, Aubry P, Fransson S-G, et al: Nephrotoxic effects in high-risk patients undergoing angiography.  N Engl J Med  2003; 348:491-499.

22. Gleeson TG, Bulugahapitiya S: Contrast-induced nephropathy.  Am J Roentgenol  2004; 183:1673-1689.

23. Heinrich MC, Kuhlmann MK, Grgic A, et al: Cytotoxic effects of ionic high-osmolar, nonionic, monomeric, and nonionic iso-osmolar dimeric iodinated contrast media on renal tubular cells in vitro.  Radiology  2005; 235:843-849.

24. Katzberg RW: Contrast medium-induced nephrotoxicity: Which pathway?.  Radiology  2005; 235:752-755.

25. Cohan RH, Dunnick NR: Intravascular contrast media: Adverse reactions.  Am J Roentgenol  1987; 149:665-670.

26. Thomsen HS: Guidelines for contrast media from the European Society of Urogenital Radiology.  Am J Roentgenol  2003; 181:1463-1471.

27. Bettmann MA, Heeren T, Greenfield A, Goudey C: Adverse events with radiographic contrast agents: Results of the SCVIR Contrast Agent Registry.  Radiology  1997; 203:611-620.

28. Rudnick MR, Goldfarb S, Wexler L, Iohexol Cooperative Study , et al: Nephrotoxicity of ionic and nonionic contrast media in 1196 patients: A randomized trial.  Kidney Int  1995; 47:254-261.

29. Ashley JB, Millward SF: Contrast agent-induced nephropathy: A simple way to identify patients with preexisting renal insufficiency.  Am J Roentgenol  2003; 181:451-454.

30. American College of Radiology Committee on Drugs and Contrast Media.  Manual on Contrast Media,  5th ed. Reston, VA, American College of Radiology, 2004.

31. Trivedi HS, Moore H, Nasr S, et al: A randomized prospective trial to assess the role of saline hydration on the development of contrast nephrotoxicity.  Nephron Clin Pract  2003; 93(1):c29-c34.

32. Tepel M, Van Der Giet M, Schwarzfeld C, et al: Prevention of radiographic-contrast-agent-induced reductions in renal function by acetylcysteine.  N Engl J Med  2000; 343:180-184.

33. Pannu N, Manns B, Lee H, Tonelli M: Systematic review of the impact of N-acetylcysteine on contrast nephropathy.  Kidney Int  2004; 65:1366-1374.

34. Merten GJ, Burgess WP, Gray LV, et al: Prevention of contrast-induced nephropathy with sodium bicarbonate: A randomized controlled trial.  JAMA  2004; 291(19):2328-2334.

35. Murphy SW, Barrett BJ, Parfrey PS: Contrast nephropathy.  J Am Soc Nephrol  2000; 11:177-182.

36. Amis ES, Hartman DS: Renal ultrasonography 1984: A practical overview.  Radiol Clin North Am  1984; 22(2):315-332.

37. Chen P, Maklad N: Redwine: Color and power Doppler imaging of the kidneys.  World J Urol  1998; 16(1):41-45.

38. Jafri SZ, Madrazo BL, Miller JH: Color Doppler ultrasound of the genitourinary tract.  Curr Opin Radiol  1992; 4(2):16-23.

39. Hricak H, Cruz C, Romanski R, et al: Renal parenchymal disease: Sonographic-histologic correlation.  Radiology  1982; 144:141-147.

40. Coleman BG: Ultrasonography of the upper genitourinary tract.  Urol Clin North Am  1985; 12(4):633-644.

41. Wells PNT: Doppler ultrasound in medical diagnosis.  Br J Radiol  1989; 62:399-420.

42. Tublin ME, Bude RO, Platt JF: Review—The resistive index in renal Doppler sonography: Where do we stand?.  Am J Roentgenol  2003; 180:885-892.

43. Keogan MT, Kliewer MA, Hertzberg BS, et al: Renal resistive indexes: Variability in Doppler US measurements in a healthy population.  Radiology  1996; 199:165-169.

44. Page JE, Morgan SH, Eastwood JB, et al: Ultrasound findings in renal parenchymal disease: Comparison with histological appearances.  Clin Radiol  1994; 49(12):867-870.

45. Hounsfield GN: Computerized transverse axial scanning (tomography): Part I. Description of system.  Br J Radiol  1973; 46:1016-1022.

46. Horton KM, Sheth S, Corl F, Fishman EK: Multidetector row CT: Principles and clinical applications.  Crit Rev Comput Tomogr  2002; 43(2):143-181.

47. Saunders HS, Dyer RB, Shifrin RY, et al: The CT nephrogram: Implications for evaluation of urinary tract disease.  RadioGraphics  1995; 15:1069-1085.

48. Perlman ES, Rosenfield AT, Wexler JS, Glockman MG: CT urography in the evaluation of urinary tract disease.  J Comput Assist Tomogr  1996; 20(4):620-626.

49. Sudakoff GS, Dunn DP, Hellman RS, et al: Opacification of the genitourinary collecting system during MDCT urography with enhanced CT digital radiography: Nonsaline versus saline bolus.  Am J Roentgenol  2006; 186:122-129.

50. Lang EK, MacChia RJ, Thomas R, et al: Improvided detection of renal pathologic features on multiphasic helical CT compared with IVU in patients presenting with microscopic hematuria.  Urology  2003; 61:528-532.

51. Kawashima A, Glockner JF, King BF: CT urography and MR urography.  Radiol Clin North Am  2003; 41:945-961.

52. McTavish JD, Jinzaki M, Zou KH, et al: Multi-detector row CT urography: Comparison of strategies for depicting the normal urinary collecting system.  Radiology  2002; 225:783-790.

53. Engelstad BL, McClennan BL, Levitt RG, et al: The role of pre-contrast images in computed tomography of the kidney.  Radiology  1980; 136:153-155.

54. McNicholas MM, Raptopoulos VD, Schwartz RK, et al: Excretory phase CT urography for opacification of the urinary collecting system.  Am J Roentgenol  1998; 170:1261-1267.

55. Caoili EM: Imaging of the urinary tract using multidetector computed tomography urography.  Semin Urol Oncol  2002; 20(3):174-179.

56. Kocakoc E, Bhatt S, Dogra VS: Renal multidetector row CT.  Radiol Clin North Am  2005; 43(6):1021-1047.

57. Caoili EM, Cohan RH, Korobkin M, et al: Urinary tract abnormalities: Initial experience with multi-detector row CT urography.  Radiology  2002; 222:353-360.

58. Joffe SA, Servaes S, Okon S, Horowitz M: Multi-detector row CT urography in the evaluation of hematuria.  RadioGraphics  2003; 23:1441-1455.

59. Schild HH: MRI made easy,  Wayne, NJ, Berlex Laboratories, Inc., 1999.

60. Hashemi RH, Bradley WG, Lisanti CJ: MRI: The Basics,  2nd ed. Philadelphia, Lippincott Williams & Wilkins, 2004.

61. Mitchell DG, Cohen MS: MRI Principles,  2nd ed. Philadelphia, Saunders, 2004.

62. Keogan MT, Edelman RR: Technologic advances in abdominal MR imaging.  Radiology  2001; 220:310-320.

63. Nelson KL, Gifford LM, Lauber-Huber C, et al: Clinical safety of gadopentetate dimeglumine.  Radiology  1995; 196:433-439.

64. Prince MR, Arnoldus C, Frisoli JK: Nephrotoxicity of high-dose gadolinium compared with iodinated contrast.  J Magn Reson Imaging  1996; 6(1):162-166.

65. Rofsky NM, Weinreb JC, Bosniak MA, et al: Renal lesion characterization with gadolinium-enhanced MR imaging: Efficacy and safety in patients with renal insufficiency.  Radiology  1991; 180:85-89.

66. Townsend RR, Cohen DL, Katholi R, et al: Safety of intravenous gadolinium (Gd-BOPTA) infusion in patients with renal insufficiency.  Am J Kidney Dis  2000; 36(6):1207-1212.

67. Sam AD, Morasch MD, Collins J, et al: Safety of gadolinium contrast angiography in patients with chronic renal insufficiency.  J Vasc Surg  2003; 38:313-318.

68. Ergün I, Keven K, Uruc I, et al: The safety of gadolinium in patients with stage 3 and 4 renal failure.  Nephrol Dial Transpl  2006; 21(3):697-700.

69. Zhang HL, Ersoy H, Prince MR: Effects of gadopentetate dimeglumine and gadodiamide on serum calcium, magnesium, and creatinine measurements.  J Magn Reson Imaging  2006; 23(3):383-387.

70. Choyke PL, Girton ME, Frank JA, et al: Clearance of gadolinium chelates by hemodialysis: An in vitro study.  J Magn Reson Imaging  2005; 5(4):470-472.

71. Grobner T: Gadolinium: a specific trigger for the development of nephrogenic fibrosing dermopathy and nephrogenic systemic fibrosis?.  Nephrol Dial Transplant  2006; 21(4):1104-1108.

72. Marckmann P, Skov L, Rossen K, et al: Nephrogenic systemic fibrosis: suspected causative role of gadodiamide used for contrast-enhanced magnetic resonance imaging.  J Am Soc Nephrol  2006; 17(9):2359-2362.

73. Maloo M, Abt P, Kashyap R, et al: Nephrogenic systemic fibrosis among liver transplant recipients: a single institution experience and topic update.  Am J Transplant  2006; 6(9):2212-2217.

74. Sadowski EA, Bennett LK, Chan MR, et al: Nephrogenic systemic fibrosis: risk factors and incidence estimation.  Radiology  2007; 243(1):148-157.

75. Broome DR, Girguis MS, Baron PW, et al: Gadodiamide-associated nephrogenic systemic fibrosis: Why radiologists should be concerned.  Am J Radiol  2007; 188:586-592.

76.   Public health advisory: gadolinium-containing contrast agents for magnetic resonance imaging (MRI)—Omniscan, OptiMARK, Magnevist, ProHance, and MultiHance. U.S. Food and Drug Administration. Published June 8, 2006. Updated December 22, 2006.

77. Cowper SE, Robin HS, Steinberg HM, et al: Scleromyxedema-like cutaneous disease in renal-dialysis patients.  Lancet  2000; 356:1000-1001.

78.   Cowper SE: Nephrogenic fibrosing dermopathy (NFD/NSF) Web site, 2001-2007. Available at http://www.icnfdr.org000672. Last accessed May 25, 2007.

79. Thomsen HS: European Society of Urogenital Radiology guidelines on contrast media application.  Curr Opin Urol  2007; 17(1):70-76.

80. Lee VS, Rofsky NM, Krinsky GA, et al: Single-dose breath-hold gadolinium-enhanced three-dimensional MR angiography of the renal arteries.  Radiology  1999; 211:69-78.

81. Kopka L, Vosshenrich R, Rodenwaldt J, Grabbe E: Differences in injection rates on contrast-enhanced breath-hold-three-dimensional MR angiography.  Am J Roentgenol  1998; 170:345-348.

82. Mitsuzaki K, Yamashita Y, Ogata I, et al: Optimal protocol for injection of contrast material at MR angiography: Study of healthy volunteers.  Radiology  1999; 213:913-918.

83. Shellock FG: Reference manual for magnetic resonance safety, implants and devices,  2006 ed. Los Angeles, Biomedical Research Publishing Company, 2006.

84. Chung JJ, Semelka RC, Martin DR: Acute renal failure: Common occurrence of preservation of corticomedullary differentiation on MR images.  Magn Reson Imaging  2001; 19(6):789-793.

85. Semelka RC, Corrigan K, Ascher SM, et al: Renal corticomedullary differentiation: Observation in patients with differing serum creatinine levels.  Radiology  1994; 190:149-152.

86. Alley MT, Shifrin RY, Pelc NJ, Herfkens RJ: Ultrafast contrast-enhanced three-dimensional MR angiography: State of the art.  RadioGraphics  1998; 18:273-285.

87. Baskaran V, Pereles FS, Nemcek AA, et al: Gadolinium-enhanced 3D MR angiography of renal artery stenosis: A pilot comparison of maximum intensity projection, multiplanar reformatting, and 3D Volume-rendering postprocessing algorithms.  Acad Radiol  2002; 9(1):50-59.

88. Prince MR, Schoenberg SO, Ward JS, et al: Hemodynamically significant atherosclerotic renal artery stenosis: MR angiographic features.  Radiology  1997; 205:128-136.

89. Willmann JK, Wildermuth S, Pfammatter T, et al: Aortoiliac and renal arteries: Prospective intraindividual comparison of contrast-enhanced three-dimensional MR angiography and multi-detector row CT angiography.  Radiology  2003; 226:798-811.

90. Jara H, Barish MA, Yucel EK, et al: MR Hydrography: Theory and practice of static fluid imaging.  Am J Roentgenol  1998; 170:873-882.

91. Nolte-Ernsting CCA, Bücker A, Adam GB, et al: Gadolinium-enhanced excretory MR urography after low-dose diuretic injection: Comparison with conventional excretory urography.  Radiology  1998; 209:147-157.

92. Sudah M, Vanninen RL, Partanen K, et al: Patients with acute flank pain: Comparison of MR urography with unenhanced helical CT.  Radiology  2002; 223:98-105.

93. Nolte-Ernsting CCA, Staatz G, Tacke J, Gunther RW: MR urography today.  Abdom Imaging  2003; 28(2):191-209.

94. El-Diasty T, Mansour O, Farouk A: Diuretic contrast-enhanced magnetic resonance Urography versus intravenous urography for depiction of nondilated urinary tracts.  Abdom Imaging  2003; 28(1):135-145.

95. Perlman SB, Bushnell DL, Barnes WE: Genitourinary System.   In: Wilson MA, ed. Textbook of Nuclear Medicine,  Philadelphia: Lippincott-Raven Publishers; 1998:117-136.

96. Mejia AA, Nakamura T, Masatoshi I, et al: Estimation of absorbed doses in humans due to intravenous administration of fluorine-18-fluorodeoxyglucose in PET studies.  J Nucl Med  1991; 32:699-706.

97. Hays MT, Watson EE, Thomas SR, et al: MIRD dose estimate report No. 19: Radiation absorbed dose estimates from 18F-FDG.  J Nucl Med  2002; 43:210-214.

98. Jones SC, Alavi A, Christman D, et al: The radiation dosimetry of 2[F-18]fluoro-2-deoxy-D-glucose in man.  J Nucl Med  1982; 23(7):613-617.

99. Kuni CC, duCret RP: Genitourinary system.  Manual of Nuclear Medicine Imaging,  New York: Thieme Medical Publishers; 1997:106-128.

100. Bagni B, Portaluppi F, Montanari L, et al: 99mTc-MAG3 versus 131I-orthoiodohippurate in the routine determination of effective renal plasma flow.  J Nucl Med Allied Sci  1990; 34(2):67-70.

101. Ritchie WW, Vick CW, Glocheski SK, Cook DE: Evaluation of azotemic patients: Diagnostic yield of initial US examination.  Radiology  1988; 167:245-247.

102. Yassa NA, Peng M, Ralls PW: Perirenal lucency (“kidney sweat”): A new sign of renal failure.  AJR Am J Roentegenol  1999; 173:1075-1077.

103. Lee JKT, Baron RL, Melson GL, et al: Can real-time ultrasonography replace static B-scanning in the diagnosis of renal obstruction?.  Radiology  1981; 139:161-165.

104. Ellenbogen PH, Schieble FW, Talner LB, Leopold GR: Sensitivity of gray scale US in detecting urinary tract obstruction.  Am J Roentgenol  1978; 130:731-733.

105. Stuck KJ, White GM, Granke DS, et al: Urinary obstruction in azotemic patients: Detection by sonography.  Am J Roentgenol  1987; 149:1191-1193.

106. Platt JF: Advances in ultrasonography of urinary tract obstruction.  Abdom Imaging  1998; 23:3-9.

107. Platt JF: Urinary obstruction.  Radiol Clin North Am  1996; 34:1113-1129.

108. Kamholtz RG, Cronan JJ, Dorfman GS: Obstruction and the minimally dilated renal collecting system: US evaluation.  Radiology  1989; 170:51-53.

109. Cronan JJ: Contemporary concepts in imaging urinary tract obstruction.  Radiol Clin North Am  1991; 29(3):527-542.

110. Mallek R, Bankier AA, Etele-Hainz A, et al: Distinction between obstructive and nonobstructive hydronephrosis: Value of diuresis duplex Doppler sonography.  Am J Roentgenol  1996; 166:113-117.

111. Scola FH, Cronan JJ, Schepps B: Grade I hydronephrosis: Pulsed Doppler US evaluation.  Radiology  1989; 171:519-520.

112. Platt JF, Rubin JM, Ellis JH, DiPietro MA: Duplex Doppler US of the kidneys: Differentiation of obstructive from nonobstructive dilatation.  Radiology  1989; 171:515-517.

113. Cronan JJ, Tublin ME: Role of the resistive index in the evaluation of acute renal obstruction.  Am J Roentgenol  1995; 164:377-378.

114. Platt JF, Ellis JH, Rubin JM: Role of renal Doppler imaging in the evaluation of acute renal obstruction.  Am J Roentgenol  1995; 164:379-380.

115. Platt JF: Looking for renal obstruction: The view from renal Doppler US.  Radiology  1994; 193:610-612.

116. Platt JF, Rubin JM, Bowerman RA, Marn CS: The inability to detect kidney disease on the basis of echogenicity.  Am J Roentgenol  1988; 151(2):317-319.

117. Gourtsoyiannis N, Prassopoulos P, Cavouras D, Pantelidis N: The thickness of the renal parenchyma decreases with age: A CT study of 360 patients.  Am J Roentgenol  1990; 155:541-544.

118. Marotti M, Hricak H, Terrier F, et al: MR in renal disease: Importance of cortical-medullary distinction.  Magn Reson Med  1987; 5:160-172.

119. Thoeny HC, De Keyzer F, Oyen RH, Peeters RR: Diffusion-weighted MR imaging of kidneys in healthy volunteers and patients with parenchymal diseases: Initial experience.  Radiology  2005; 235:911-917.

120. Hauger O, Frost EE, van Heeswijk R, et al: MR Evaluation of the glomerular homing of magnetically labeled mesenchymal stem cells in a rat model of nephropathy.  Radiology  2006; 238(1):200-210.

121. Lin EC, Gellens ME, Goodgold HM: Prognostic value of renal scintigraphy with Tc-99m MAG3 in patients with acute renal failure.  J Nucl Med  1995; 36:232P-233P.

122. Saremi F, Jadvar H, Siegel M: Pharmacologic interventions in nuclear radiology: Indications, imaging protocols, and clinical results.  Radiographics  2002; 22(3):477-490.

123. Kuni CC, duCret RP: Genitourinary system.  Manual of Nuclear Medicine Imaging,  New York: Thieme Medical Publishers; 1997:106-128.

124. Dyer RB, Chen MYM, Zagoria RJ: Abnormal calcifications in the urinary tract.  RadioGraphics  1998; 18:1405-1424.

125. Ginalski JM, Portmann L, Jaeger PH: Does medullary sponge kidney cause nephrolithiasis?.  Am J Roentgenol  1990; 155:299-302.

126. Gibson MS, Puckett ML, Shelly ME: Renal tuberculosis.  RadioGraphics  2004; 24:251-256.

127. Clark JY, Thompson IM, Optenberg SA: Economic impact of urolithiasis in the United States.  J Urol  1995; 154:2020-2042.

128. Tublin ME, Murphy ME, Delong DM, et al: Conspicuity of renal calculi at unenhanced CT: Effects of calculus composition and size and CT technique.  Radiology  2002; 225:91-96.

129. Newhouse JH, Prien EL, Amis ES, et al: Computed tomographic analysis of urinary calculi.  Am J Roentgenol  1984; 142:545-548.

130. Hillman BJ, Drach GW, Tracey P, Gaines JA: Computed tomographic analysis of renal calculi.  Am J Roentgenol  1984; 142:549-552.

131. Mostafavi MR, Ernst RD, Saltzman B: Accurate determination of chemical composition of urinary calculi by spiral computerized tomography.  J Urol  1998; 159(3):673-675.

132. Smith RC, Rosenfield AT, Choe KA, et al: Acute flank pain: Comparison of non-contrast-enhanced CT and intravenous urography.  Radiology  1995; 194:789-794.

133. Haddad MC, Sharif HS, Abomelha MS, et al: Management of renal colic: Redefining the role of the urogram.  Radiology  1992; 184(1):35-36.

134. Coll DM, Varanelli MJ, Smith RC: Relationship of spontaneous passage of ureteral calculi to stone size and location as revealed by unenhanced helical CT.  Am J Roentgenol  2002; 178:101-103.

135. Smith RC, Varanelli M: Diagnosis and management of acute ureterolithiasis.  Am J Roentgenol  2000; 175:3-6.

136. Middleton WD, Dodds WJ, Lawson TL, Foley WD: Renal calculi: Sensitivity for detection with US.  Radiology  1988; 167:239-244.

137. Gottlieb RH, La TC, Erturk EN, et al: CT in detecting urinary tract calculi: Influence on patient imaging and clinical outcomes.  Radiology  2002; 225:441-449.

138. Sourtzis S, Thibeau JF, Damry N, et al: Radiologic investigation of renal colic: Unenhanced helical CT compared with excretory urography.  Am J Roentgenol  1999; 172:1491-1494.

139. Boulay I, Holtz P, Foley WD, et al: Ureteral calculi: Diagnostic efficacy of helical CT and implications for treatment of patients.  Am J Roentgenol  1999; 172:1485-1490.

140. Katz DS, Hines J, Rausch DR, et al: Unenhanced helical CT for suspected renal colic.  Am J Roentgenol  1999; 173:425-430.

141. Haddad MC, Sharif HS, Shahed MS, et al: Renal colic: Diagnosis and outcome.  Radiology  1992; 184:83-88.

142. Smith RC, Rosenfield AT, Choe KA, et al: Acute flank pain: Comparison of non-contrast-enhanced CT and intravenous urography.  Radiology  1995; 194:789-794.

143. Flowler KAB, Locken JA, Duchesne JH, Williamson MR: US for detecting renal calculi with nonenhanced CT as a reference standard.  Radiology  2002; 222:109-113.

144. Catalano O, Nunziata A, Altei F, Siani A: Suspected ureteral colic: Primary helical CT versus selective helical CT after unenhanced radiography and sonography.  Am J Roentgenol  2002; 178:379-387.

145. Rucker CM, Menias CO, Bhalla S: Mimics of renal colic: Alternative diagnoses at unenhanced helical CT.  RadioGraphics  2004; 24:S11-S33.

146. Tamm EP, Silverman PM, Shuman WP: Evaluation of the patient with flank pain and possible ureteral calculus.  Radiology  2003; 228:319-329.

147. Diel J, Perlmutter S, Venkataramanan , et al: Unenhanced helical CT using increased pitch for suspected renal colic: An effective technique for radiation dose reduction?.  J Computer Assist Tomogr  2000; 24:795-801.

148. Katz DS, Venkataramanan , Napel S, Sommer FG: Can low-dose unenhanced multidetector CT be used for routine evaluation of suspected renal colic?.  Am J Roentgenol  2003; 180:313-315.

149. Saw KC, McAteer JA, Monga AG, et al: Helical CT of urinary calculi: Effect of stone composition, stone size, and scan collimation.  Am J Roentgenol  2000; 175:329-332.

150. Nadler RB, Rubenstein JN, Eggener SE, et al: The etiology of urolithiasis in HIV infected patients.  J Urol  2003; 169:475-477.

151. Blake SP, McNicholas MMJ, Raptopoulos V: Nonopaque crystal deposition causing ureteric obstruction in patients with HIV undergoing indinavir therapy.  Am J Roentgenol  1998; 171:717-720.

152. Boridy IC, Kawashima A, Goldman SM, Sandler CM: Acute uroterolithiasis: Nonenhanced helical CT findings of perinephric edema for prediction of degree of ureteral obstruction.  Radiology  1999; 213:663-667.

153. Georgiades CS, Moore CJ, Smith DP: Differences of renal parenchymal attenuation for acutely obstructed and unobstructed kidneys on unenhanced helical CT: A useful secondary sign?.  Am J Roentgenol  2001; 176:965-968.

154. Goldman SM, Faintuch S, Ajzen SA, et al: Diagnostic value of attenuation measurements of the kidney on unenhanced helical CT of obstructive ureterolithiasis.  Am J Roentgenol  2004; 182:1251-1254.

155. Narepalem N, Sundaram CP, Boridy IC, et al: Comparison of helical computerized tomography and plain radiography for estimating urinary stone size.  J Urol  2002; 167(3):1235-1238.

156. Takahashi N, Kawashima A, Ernst RD, et al: Ureterolithiasis: Can clinical outcome be predicted with unenhanced helical CT?.  Radiology  1998; 208:97-102.

157. Dalrymple NC, Casford B, Raiken DP, et al: Pearls and pitfalls in the diagnosis of ureterolithiasis with unenhanced helical CT.  RadioGraphics  2000; 20:439-447.

158. Sudah M, Vanninen RL, Partanen K, et al: Patients with acute flank pain: Comparison of MR urography with unenhanced helical CT.  Radiology  2002; 223:98-105.

159. Regan F, Bohlman ME, Khazan R, et al: MR urography using HASTE imaging in the assessment of ureteric obstruction.  Am J Roentgenol  1996; 167:1115-1120.

160. Ku JH, Jeon YS, Kim ME, et al: Is there a role for magnetic resonance imaging in renal trauma?.  Int J Urol  2001; 8:261-267.

161. Talner LB, Davidson AJ, Lebowitz RL, et al: Acute pyelonephritis: Can we agree on terminology?.  Radiology  1994; 192:297-305.

162. Papanicolaou N, Pfister RC: Acute renal infections.  Radiol Clin North Am  1996; 34(5):965-995.

163. Hamper UM, Goldblum LE, Hutchins GM, et al: Renal involvement in AIDS: Sonographic-pathologic correlation.  Am J Roentgenol  1988; 150:1321-1325.

164. Koh DM, Langroudi B, Padley SPG: Abdominal CT in patients with AIDS Imaging.  Br Inst Radiol  2002;24-34.

165. Kay CJ: Renal diseases in patients with AIDS: Sonographic findings.  Am J Roentgenol  1992; 159:551-554.

166. Grayson DE, Abbott RM, Levy AD, et al: Emphysematous infections of the abdomen and pelvis: A pictorial review.  RadioGraphics  2002; 22:543-561.

167. Rodriguez-de-Velasquez A, Yoder IC, Velasquez PA, Papanicolaou N: Imaging the effects of diabetes on the genitourinary system.  RadioGraphics  1995; 15:1051-1068.

168. Hayes WS, Hartman DS, Sesterbenn I: From the archives of the AFIP. Xanthogranulomatous pyelonephritis.  RadioGraphics  1991; 11:485-498.

169. Kenney PJ: Imaging of chronic renal infections.  Am J Roentgenol  1990; 155:485-494.

170. Soulen MC, Fishman EK, Goldman SM, Gatewood OMB: Bacterial renal infection: Role of CT.  Radiology  1989; 171:703-707.

171. Sheth S, Fishman EK: Multi-detector row CT of the kidneys and urinary tract: Techniques and applications in the diagnosis of benign diseases.  RadioGraphics  2004; 24:e20.

172. Kawashima A, Sandler CM, Goldman SM, et al: CT of renal inflammatory disease.  RadioGraphics  1997; 17:851-866.

173. Gervais DA, Shitman GJ: Emphysematous pyelonephritis.  Am J Roentgenol  1994; 162:348.

174. Wan Y-L, Lee T-Y, Bullard MJ, Tsai C-C: Acute gas-producing bacterial renal infection: Correlation between imaging findings and clinical outcome.  Radiology  1996; 198:433-438.

175. Roy C, Pfleger DD, Tuchmann CM, et al: Emphysematous pyelitis: Findings in five patients.  Radiology  2001; 218:647-650.

176. Fan CM, Whitman GJ, Chew FS: Xanthogranulomatous pyelonephritis.  Am J Roentgenol  1995; 165:862.

177. Majd M, Blask ARN, Markle BM, et al: Acute pyelonephritis: Comparison of diagnosis with 99mTc-DMSA SPECT, spiral CT, MR imaging, and power Doppler US in an experimental pig model.  Radiology  2001; 218:101-108.

178. Bjorgvinsson E, Majd M, Eggli KD: Diagnosis of acute pyelonephritis in children: Comparison of sonography and 99mTc-DMSA scintigraphy.  Am J Roentgenol  1991; 157:539-543.

179. Warshauer DM, McCarthy SM, Street L, et al: Detection of renal masses: Sensitivities and specificities of excretory urography/linear tomography, US, and CT.  Radiology  1988; 169:363-365.

180. Bosniak , Morton A: The use of the Bosniak classification system for renal cysts and cystic tumors.  J Urol  1997; 157(5):1852-1853.

181. Jinzaki M, McTavish JD, Zou KH, et al: Evaluation of small (≤ 3 cm) renal masses with MDCT: Benefits of thin overlapping reconstructions.  Am J Roentgenol  2004; 183:223-228.

182. Silverman SG, Lee BY, Seltzer SE, et al: Small (≤ 3 cm) renal masses: Correlation of spiral CT features and pathologic findings.  Am J Roentgenol  1994; 163:597-605.

183. Hayden CK, Swischuk LE, Smith TH, Armstrong EA: Renal cystic disease in childhood.  RadioGraphics  1986; 6(1):97-116.

184. Lonergan GF, Rice RR, Suarez ES: Autosomal recessive polycystic kidney disease: Radiologic-pathologic correlation.  RadioGraphics  2000; 20:837-855.

185. Walker FC, Loney LC, Root ER, et al: Diagnostic evaluation of adult polycystic kidney disease in childhood.  Am J Roentgenol  1984; 142:1273-1277.

186. Nicolau C, Torra R, Badenas C, et al: Autosomal dominant polycystic kidney disease types 1 and 2: Assessment of US sensitivity for diagnosis.  Radiology  1999; 213:273-276.

187. Heinz-Peer G, Schoder M, Rand T, et al: Prevalence of acquired cystic kidney disease and tumors in native kidneys of renal transplant recipients: A prospective US study.  Radiology  1995; 195:667-671.

188. Levine E: Acquired cystic kidney disease.  Radiol Clin North Am  1996; 34(5):947-964.

189. Levine E, Slusher SL, Grantham JJ, Wetzel LH: Natural history of acquired renal cystic disease in dialysis patients: A prospective longitudinal CT study.  Am J Roentgenol  1991; 156:501-506.

190. Takebayashi S, Hidai H, Chiba T, et al: Using helical CT to evaluate renal cell carcinoma in patients undergoing hemodialysis: Value of early enhanced images.  Am J Roentgenol  1999; 172:429-433.

191. Taylor AJ, Cohen EP, Erickson SJ, et al: Renal imaging in long-term dialysis patients: A comparison of CT and sonography.  Am J Roentgenol  1989; 153:765-767.

192. Takase K, Takahashi S, Tazawa S, et al: Renal cell carcinoma associated with chronic renal failure: Evaluation with sonographic angiography.  Radiology  1994; 192:787-792.

193. Siegel SC, Sandler MA, Alpern MB, Pearlberg JL: CT of renal cell carcinoma in patients on chronic hemodialysis.  Am J Roentgenol  1988; 150:583-585.

194. Matson MA, Cohen EP: Acquired cystic kidney disease: Occurrence, prevalence, and renal cancers.  Medicine  1990; 69(4):217-226.

195. Choyke PL, Glenn GM, Walther MM, et al: Hereditary renal cancers.  Radiology  2003; 226:33-46.

196. Bosniak MA: State of the Art. The current radiological approach to renal cysts.  Radiology  1986; 158:1-10.

197. Zagoria RJ: Imaging of small renal masses: A medical success story.  Am J Roentgenol  2000; 175:945-955.

198. Lowe LH, Isuani BH, Heller RM, et al: Pediatric renal masses: Wilms tumor and beyond.  RadioGraphics  2000; 20:1585-1603.

199. Wagner BJ, Maj MC, Wong-You-Cheong JJ, Davis CJ: Adult renal hamartomas.  RadioGraphics  1997; 17:155-169.

200. Bosniak MA, Megibow AJ, Hulnick DH, et al: CT diagnosis of renal angiomyolipoma: The importance of detecting small amounts of fat.  Am J Roentgenol  1988; 151:497-501.

201. Silverman SG, Pearson GDN, Seltzer SE, et al: Small (≤ 3 cm) hyperechoic renal masses: Comparison of helical and conventional CT for diagnosing angiomyolipoma.  Am J Roentgenol  1996; 167:877-881.

202. Siegel CL, Middleton WD, Teefey SA, McClennan BL: Angiomyolipoma and renal cell carcinoma: US differentiation.  Radiology  1996; 198:789-793.

203. Kim JK, Park SY, Shon JH, Cho KS: Angiomyolipoma with minimal fat: Differentia-tion from renal cell carcinoma at biphasic helical CT.  Radiology  2004; 230:677-684.

204. Jinzaki M, Tanimoto A, Narimatsu Y, et al: Angiomyolipoma: Imaging findings in lesions with minimal fat.  Radiology  1997; 205:497-502.

205. Lesavre A, Correas JM, Merran S, et al: CT of papillary renal cell carcinomas with cholesterol necrosis mimicking angiomyolipomas.  Am J Roentgenol  2003; 181:143-145.

206. Israel GM, Bosniak MA, Slywotzky CM, Rosen RJ: CT differentiation of large exophytic renal angiomyolipomas and perirenal liposarcomas.  Am J Roentgenol  2002; 179:769-773.

207. Bosniak M, Megibow AJ, Hulnick DH, et al: CT diagnosis of renal angiomyolipoma: The importance of detecting small amounts of fat.  Am J Roentgenol  1988; 151:497-501.

208. Lemaitre L, Robert Y, Dubrulle F, et al: Renal angiomyolipoma: Growth followed up with CT and/or US.  Radiology  1995; 197:598-602.

209. Yamakado K, Tanaka N, Nakagawa T, et al: Renal angiomyolipoma: Relationships between tumor size, aneurysm formation, and rupture.  Radiology  2002; 225:78-82.

210. Palmer WE, Chew FS: Renal oncocytoma.  Am J Roentgenol  1991; 156:1144.

211. Levine E, Huntrakoon M: Computed tomography of renal oncocytoma.  Am J Roentgenol  1983; 141(4):741-746.

212. On the Am J Roentgenol Viewbox. Renal oncocytoma displaying intense activity on 18F-FDG PET.  Am J Roentgenol  2006; 186:269-271.

213. Neisius D, Braedel HU, Schindler E, et al: Computed tomographic and angiographic findings in renal oncocytoma.  Br J Radiol  1988; 61(731):1019-1025.

214. Davidson AJ, Hayes WS, Hartman DS, et al: Renal oncocytoma and carcinoma: Failure of differentiation with CT.  Radiology  1993; 186:693-696.

215. Curry NS, Schabel SI, Garvin AJ, Fish G: Case Report. Intratumoral fat in a renal oncocytoma mimicking angiomyolipoma.  Am J Roentgenol  1990; 154:307-308.

216. Bostwick DG, Eble JN, Murphy GP: Conference summary. Diagnosis and prognosis of renal cell carcinoma: 1997 Workshop, Rochester, Minnesota, March 21-22, 1997.  Cancer  1997; 80(5):975-976.

217. Bonsib SM: Risk and prognosis in renal neoplasms. A pathologist's prospective.  Urol Clin North Am  1999; 26(3):643-660.

218. Russo P: Renal cell carcinoma: Presentation, staging, and surgical treatment.  Semin Oncol  2000; 27(2):160-176.

219. Sheth S, Scatarige JC, Horton KM, et al: Current concepts in the diagnosis and management of renal cell carcinoma: Role of multidetector CT and three-dimensional CT.  RadioGraphics  2001; 21:S237-S254.

220. Coll DM, Herts BR, Davros WJ, et al: Preoperative use of 3D volume rendering to demonstrate renal tumors and renal anatomy.  RadioGraphics  2000; 20:431-438.

221. Gervais DA, McGovern FJ, Arellano RS, et al: Renal cell carcinoma: Clinical experience and technical success with radio-frequency ablation of 42 tumors.  Radiology  2003; 226:417-424.

222. Mayo-Smith WW, Dupuy DE, Parikh PM, et al: Imaging-guided percutaneous radiofrequency ablation of solid renal masses: Techniques and outcomes of 38 treatment sessions in 32 consecutive patients.  Am J Roentgenol  2003; 180:1503-1508.

223. Zagoria RF: Imaging-guided radio-frequency ablation of renal masses.  RadioGraphics  2004; 24:S59-S71.

224. Suh RD, Goldin JG, Wallace AB, et al: Metastatic renal cell carcinoma: CT-guided immunotherapy as a technically feasible and safe approach to delivery of gene therapy for treatment.  Radiology  2004; 231:359-364.

225. Jamis-Dow CA, Choyke PL, Jennings SB, et al: Small (<3-cm) renal masses: Detection with CT versus US and pathologic correlation.  Radiology  1996; 198:785-788.

226. Jinzaki M, Ohkuma K, Tanimoto A, et al: Small solid renal lesions: Usefulness of power Doppler US.  Radiology  1998; 209:543-550.

227. Forman HP, Middleton WD, Melson GL, McClennan BL: Hyperechoic renal cell carcinomas: Increase in detection at US.  Radiology  1993; 188:431-434.

228. Ascenti G, Gaeta M, Magno C, et al: Contrast-enhanced second-harmonic sonography in the detection of pseudocapsule in renal cell carcinoma.  Am J Roentgenol  2004; 182:1525-1530.

229. Schmidt T, Hohl C, Haage P, et al: Diagnostic accuracy of phase-inversion tissue harmonic imaging versus fundamental B-mode sonography in the evaluation of focal lesions of the kidney.  Am J Roentgenol  2003; 180:1639-1647.

230. Davidson AJ, Hartman DS, Choyke PL, Wagner BJ: Radiologic assessment of renal masses: Implications for patient care.  Radiology  1997; 202:297-305.

231. Yuh BI, Cohan RH: Different phases of renal enhancement: Role in detecting and characterizing renal masses during helical CT.  Am J Roentgenol  1999; 173:747-755.

232. Cohan RH, Sherman LS, Korobkin M, et al: Renal masses: Assessment of corticomedullary-phase and nephrographic-phase CT scans.  Radiology  1995; 196:445-451.

233. Suh M, Coakley FV, Qayyum A, et al: Distinction of renal cell carcinomas from high-attenuation renal cysts at portal venous phase contrast-enhanced CT.  Radiology  2003; 228:330-334.

234. Birnbaum BA, Jacobs JE, Ramchandani P: Multiphasic renal CT: Comparison of renal mass enhancement during the corticomedullary and nephrographic phases.  Radiology  1996; 200:753-758.

235. Kopka L, Fischer U, Zoeller G, et al: Dual-phase helical CT of the kidney: Value of the corticomedullary and nephrographic phase for evaluation of renal lesions and preoperative staging of renal cell carcinoma.  Am J Roentgenol  1997; 169:1573-1578.

236. Macari M, Bosniak MA: Delayed CT to evaluate renal masses incidentally discovered at contrast-enhanced CT: Demonstration of vascularity with deenhancement.  Radiology  1999; 213:674-680.

237. Zeman RK, Zeiberg A, Hayes WS, et al: Helical CT of renal masses: The value of delayed scans.  Am J Roentgenol  1996; 167:771-776.

238. Benjaminov O, Atri M, O'Malley M, et al: Enhancing component on CT to predict malignancy in cystic renal masses and interobserver agreement of different CT features.  Am J Roentgenol  2006; 186:665-672.

239. Ruppert-Kohlmayr AJ, Uggowitzer M, Meissnitzer T, Ruppert G: Differentiation of renal clear cell carcinoma and renal papillary carcinoma using quantitative CT enhancement parameters.  Am J Roentgenol  2004; 183:1387-1391.

240. Kim JK, Kim TK, Ahn HJ, et al: Differentiation of subtypes of renal cell carcinoma on helical CT scans.  Am J Roentgenol  2002; 178:1499-1506.

241. Browne RFJ, Meehan CP, Colville J, et al: Transitional cell carcinoma of the upper urinary tract: Spectrum of imaging findings.  RadioGraphics  2005; 25:1609-1627.

242. Pickhardt PF, Lonergan GF, Davis CF, et al: From the archives of the AFIP. Infiltrative renal lesions: Radiologic-pathologic correlation.  RadioGraphics  2000; 20:215-243.

243. Urban BA, Fishman EK: Renal lymphoma: CT patterns with emphasis on helical CT.  RadioGraphics  2000; 20:197-212.

244. Hartman DS, Choyke PL, Hartman MS: From the RSNA refresher courses. A practical approach to the cystic renal mass.  RadioGraphics  2004; 24:S101-S115.

245. Israel GM, Hindman N, Bosniak MA: Evaluation of cystic renal masses: Comparison of CT and MR imaging by using the Bosniak classification system.  Radiology  2004; 231:365-371.

246. Siegel CL, McFarland EG, Brink JA, et al: CT of cystic renal masses: Analysis of diagnostic performance and interobserver variation.  Am J Roentgenol  1997; 169:813-818.

247. Israel GM, Bosniak MA: Follow-up CT of moderately complex cystic lesions of the kidney (Bosniak Category IIF).  Am J Roentgenol  2003; 181:627-633.

248. Curry NS, Cochran ST, Bissada NK: Cystic renal masses: Accurate Bosniak classification requires adequate renal CT.  Am J Roentgenol  2000; 175:339-342.

249. Harisinghani MG, Maher MM, Gervais DA, et al: Incidence of malignancy in complex cystic renal masses (Bosniak Category III): Should imaging-guided biopsy precede surgery?.  Am J Roentgenol  2003; 180:755-758.

250. Dechet CB, Sebo T, Farrow G, et al: Prospective analysis of intraoperative frozen needle biopsy of solid renal masses in adults.  J Urol  1999; 162:1282-1285.

251. Wood BJ, Khan MA, McGovern F, et al: Imaging guided biopsy of renal masses: Indications, accuracy and impact on clinical management.  J Urol  1999; 161:1470-1474.

252. Rybicki FJ, Shu KM, Cibas ES, et al: Percutaneous biopsy of renal masses: Sensitivity and negative predictive value stratified by clinical setting and size of masses.  Am J Roentgenol  2003; 180:1281-1287.

253. Israel GM, Hindman N, Bosniak MA: Evaluation of cystic renal masses: Comparison of CT and MR imaging by using the Bosniak classification system.  Radiology  2004; 231:365-371.

254. Semelka RC, Shoenut JP, Kroeker MA, et al: Renal lesions: Controlled comparison between CT and 1.5-T MR imaging with nonenhanced and gadolinium-enhanced fat-suppressed spin-echo and breath-hold FLASH techniques.  Radiology  1992; 182:425-430.

255. Hecht EM, Israel GM, Krinsky GA, et al: Renal masses: Quantitative analysis of enhancement with signal intensity measurements versus qualitative analysis of enhancement with image subtraction for diagnosing malignancy at MR imaging.  Radiology  2004; 232:373-378.

256. Farres MT, Ronco P, Saadoun D, et al: Chronic lithium nephropathy: MR imaging for diagnosis.  Radiology  2003; 229:570-574.

257. Israel GM, Hindman N, Hecht E, Krinsky G: The use of opposed-phase chemical shift MRI in the diagnosis of renal angiomylipomas.  Am J Roentgenol  2005; 184:1868-1872.

258. Yoshimitsu K, Kakihara D, Irie H, et al: Papillary renal carcinoma: Diagnostic approach by chemical shift gradient-echo and echo-planar MR imaging.  J Magn Reson Imaging  2006; 23(3):339-344.

259. Ergen FB, Hussain HK, Caoili EM, et al: MRI for preoperative staging of renal cell carcinoma using the 1997 TNM classification: Comparison with surgical and pathologic staging.  Am J Roentgenol  2004; 182:217-225.

260. Roy C, El Ghali S, Buy X, et al: Significance of the pseudocapsule on MRI of renal neoplasms and its potential application for local staging: A retrospective study.  Am J Roentgenol  2005; 184:113-120.

261. Choyke PL, Walther MM, Wagner JR: Renal cancer: Preoperative evaluation with dual-phase three-dimensional MR angiography.  Radiology  1997; 205:767-771.

262. El-Galley R: Surgical management of renal tumors.  Radiol Clin North Am  2003; 41:1053-1065.

263. Semelka RC, Kelekis NL, Burdeny DA, et al: Renal lymphoma: Demonstration by MR imaging.  Am J Roentgenol  1996; 166:823-827.

264. Frank IN, Graham Jr S, Nabors WL: Urologic and male genital cancers.   In: Holleb AI, Fink DJ, Murphy GP, ed. Clinical Oncology,  American Cancer Society; 1991:272-274.

265. Goldberg MA, Mayo-Smith WW, Papanicolaou N, et al: FDG PET characterization of renal masses: Preliminary experience.  Clin Radiol  1997; 52:510-515.

266. Jadvar H, Kherbache HM, Pinski JK, Conti PS: Diagnostic role of [F-18]-FDG positron emission tomography in restaging renal cell carcinoma.  Clin Nephrol  2003; 60:395-400.

267. Mankoff DA, Thompson JA, Gold P, et al: Identification of interleukin-2-induced complete response in metastatic renal cell carcinoma by FDG PET despite radiographic evidence suggesting persistent tumor.  Am J Roentgenol  1997; 169:1049-1050.

268. Ramdave S, Thomas GW, Berlangieri SU, et al: Clinical role of F-18 fluorodeoxyglucose positron emission tomography for detection and management of renal cell carcinoma.  J Urol  2001; 166:825-830.

269. Wahl RL, Harney J, Hutchins G, Grossman HB: Imaging of renal cancer using positron emission tomography with 2-deoxy-2-(18f)-fluoro-D-glucose: Pilot animal and human studies.  J Urol  1991; 146(6):1470-1474.

270. Wu HC, Yen RF, Shen YY, et al: Comparing whole body 18F-2-deoxyglucose positron emission tomography and technetium-99m methylene diphosphate bone scan to detect bone metastases in patients with renal cell carcinomas—A preliminary report.  J Cancer Res Clin Oncol  2002; 128:503-506.

271. Majhail NS, Urbain JL, Albani JM, et al: F-18 Fluorodeoxyglucose positron emission tomography in the evaluation of distant metastases from renal cell carcinoma.  J Clin Oncol  2003; 21:3995-4000.

272. Seto E, Segall GM, Terris MK: Positron emission tomography detection of osseous metastases of renal cell carcinoma not identified on bone scan.  Urology  2000; 55:286.

273. Zhuang H, Duarte PS, Pourdehand M, et al: Standardized uptake value as an unreliable index of renal disease on fluorodeoxyglucose PET imaging.  Clin Nucl Med  2000; 25:358-360.

274. Kang DE, White Jr RL, Zuger JH, et al: Clinical use of fluorodeoxyglucose F 18 positron emission tomography for detection of renal cell carcinoma.  J Urol  2004; 171(5):1806-1809.

275. Safaei A, Figlin R, Hoh CK, et al: The usefulness of F-18 deoxyglucose whole-body positron emission tomography (PET) for re-staging of renal cell cancer.  Clin Nephrol  2002; 57:56-62.

276. Miyakita H, Tokunaga M, Onda H, et al: Significance of 18F-fluorodeoxyglucose positron emission tomography (FDG-PET) for detection of renal cell carcinoma and immunohistochemical glucose transporter 1 (GLUT-1) expression in the cancer.  Int J Urol  2002; 9:15-18.

277. Nagase Y, Takata K, Moriyama N, et al: Immunohistochemicallocalization of glucose transporters in human renal cell carcinoma.  J Urol  1995; 153(3 Pt 1):798-801.

278. Kumar R, Chauhan A, Lakhani P, et al: 2-Deoxy-2-[F-18]Fluoro-D-Glucose-Positron emission tomography in characterization of solid renal masses.  Mol Imaging Biol  2005; 7(6):431-439.

279. Shreve P, Chiao PC, Humes HD, et al: Carbon-11-acetate PET imaging in renal disease.  J Nucl Med  1995; 36:1595-1601.

280. Lawrentschuk N, Poon AM, Foo SS, et al: Assessing regional hypoxia in human renal tumors using 18F-Fluoromisonidazole positron emission tomography.  BJU Int  2005; 96(4):540-546.

281. Hillman BJ: Imaging advances in the diagnosis of renovascular hypertension.  Am J Roentgenol  1989; 153:5-14.

282. Albers FJ: Clinical characteristics of atherosclerotic renovascular disease.  Am J Kidney Dis  1994; 24(4):636-641.

283. Ota H, Takase K, Rikimaru H, et al: Quantitative vascular measurements in arterial occlusive disease.  RadioGraphics  2005; 25:1141-1158.

284. Siegel CL, Ellis JH, Korobkin M, Dunnick NR: CT-Detected renal arterial calcification: Correlation with renal artery stenosis on angiography.  Am J Roentgenol  1994; 163:867-872.

285. Beregi JP, Louvegny S, Gautier C, et al: Fibromuscular dysplasia of the renal arteries: Comparison of helical CT angiography and arteriography.  Am J Roentgenol  1999; 172:27-34.

286. Bolduc JP, Oliva VL, Therasse E, et al: Diagnosis and treatment of renovascular hypertension: A cost-benefit analysis.  Am J Roentgenol  2005; 184:931-937.

287. Soulez G, Oliva VL, Turpin S, et al: Imaging of renovascular hypertension: Respective values of renal scintigraphy, renal Doppler US, and MR angiography.  RadioGraphics  2000; 20:1355-1368.

288. Desberg AL, Paushter DM, Lammert GK, et al: Renal artery stenosis: Evaluation with color Doppler flow imaging.  Radiology  1990; 177:749-753.

289. Hamper UM, DeJong MR, Caskey CI, Sheth S: Power Doppler imaging: Clinical experience and correlation with color Doppler US and other imaging modalities.  RadioGraphics  1977; 17:499-513.

290. Helenon O, El Rody F, Correas JM, et al: Color Doppler US of renovascular disease in native kidneys.  RadioGraphics  1995; 15:833-854.

291. Halpern EJ, Needleman L, Nack TL, East SA: Renal artery stenosis: Should we study the main renal artery or segmental vessels?.  Radiology  1995; 195:799-804.

292. House MK, Dowling RJ, King P, Gibson RN: Using Doppler sonography to reveal renal artery stenosis: An evaluation of optimal imaging parameters.  Am J Roentgenol  1999; 173:761-765.

293. Kliewer MA, Tupler RH, Carroll BA, et al: Renal artery stenosis: Analysis of Doppler waveform parameters and Tardus-Parvus pattern.  Radiology  1993; 189:779-787.

294. Melany ML, Grant EG, Duerinckx AJ, et al: Ability of a phase shift US contrast agent to improve imaging of the main renal arteries.  Radiology  1997; 205:147-152.

295. Claudon M, Plouin PF, Baxter GM, et al: Renal arteries in patients at risk of renal arterial stenosis: Multicenter evaluation of the echo-enhancer SH U 508A at color and spectral Doppler US.  Radiology  2000; 214:739-746.

296. Urban BA, Ratner LE, Fishman EK: Three-dimensional volume-rendered CT angiography of the renal arteries and veins: Normal anatomy, variants, and clinical applications.  RadioGraphics  2001; 21:373-386.

297. Kaatee R, Beek FJA, DeLange EE, et al: Renal artery stenosis: Detection and quantification with spiral CT angiography versus optimized digital subtraction angiography.  Radiology  1997; 205:121-127.

298. Beregi JP, Elkohen M, Deklunder G, et al: Helical CT angiography compared with arteriography in the detection of renal artery stenosis.  Am J Roentgenol  1996; 167:495-501.

299. Kawashima A, Sandler CM, Ernst RD, et al: CT evaluation of renovascular disease.  RadioGraphics  2000; 20:1321-1340.

300. Rubin GD, Dake MD, Napel S, et al: Spiral CT of renal artery stenosis: Comparison of three-dimensional rendering techniques.  Radiology  1994; 190:181-189.

301. Brink JA, Lim JT, Wang G, et al: Technical optimization of spiral CT for depiction of renal artery stenosis: In vitro analysis.  Radiology  1995; 194:157-163.

302. Bude RO, Forauer AR, Caoili EM, Nghiem HV: Is it necessary to study accessory arteries when screening the renal arteries for renovascular hypertension?.  Radiology  2003; 226:411-416.

303. Mallouhi A, Rieger M, Czermak B, et al: Volume-rendered multidetector CT angiography: Noninvasive follow-up of patients treated with renal artery stents.  Am J Roentgenol  2003; 180:233-239.

304. Behar JV, Nelson RC, Zidar JP, et al: Thin-section multidetector CT angiography of renal artery stents.  Am J Roentgenol  2002; 178:1155-1159.

305. Willmann J, Wildermuth S, Pfammatter T, et al: Aortoiliac and renal arteries: Prospective intraindividual comparison of contrast-enhanced three-dimensional MR angiography and multi-detector row CT angiography.  Radiology  2003; 226:798-811.

306. Thornton MJ, Thornton F, O'Callaghan J, et al: Evaluation of dynamic gadolinium-enhanced breath-hold MR angiography in the diagnosis of renal artery stenosis.  Am J Roentgenol  1999; 173:1279-1283.

307. Qanadli SD, Soulez G, Therasse E, et al: Detection of renal artery stenosis: Prospective comparison of captopril-enhanced Doppler sonography, captopril-enhanced scintigraphy, and MR angiography.  Am J Roentgenol  2001; 177:1123-1129.

308. Mallouhi A, Schocke M, Judmaier W, et al: 3D MR angiography of renal arteries: Comparison of volume rendering and maximum intensity projection algorithms.  Radiology  2002; 223:509-516.

309. Schoenberg SO, Knopp MV, Londy F, et al: Morphologic and functional magnetic resonance imaging of renal artery stenosis: A multireader tricenter study.  J Am Soc Nephrol  2002; 13:158-169.

310. Soulez G, Olivia VL, Turpin S, et al: Imaging of renovascular hypertension: Respective values of renal scintigraphy, renal Doppler US and MR angiography.  RadioGraphics  2000; 20:1355-1368.

311. Bude RO, Forauer AR, Caoili EM, Nghiem HV: Is it necessary to study accessory arteries when screening the renal arteries for renovascular hypertension?.  Radiology  2003; 226:411-416.

312. Wilson GJ, Hoogeveen RM, Willinek WA, et al: Parellel imaging in MR angiography.  Top Magn Reson Imaging  2004; 15(3):169-185.

313. Gutberlet M, Noeske R, Schwinge K, et al: Comprehensive cardiac magnetic resonance imaging at 3.0 tesla: Feasibility and implications for clinical applications.  Invest Radiol  2006; 41(2):154-167.

314. Chen Q, Quijano CV, Mai VM, et al: On improving temporal and spatial resolution of 3D contrast-enhanced body MR angiography with parallel imaging.  Radiology  2004; 231:893-899.

315. de Haan MW, van Engelshoven JMA, Houben AJHM, et al: Phase-contrast magnetic resonance flow quantification in renal arteries comparison with 133 Xenon washout measurements.  Hypertension  2003; 41:114-118.

316. Schoenberg SO, Knopp MV, Londy F, et al: Morphologic and functional magnetic resonance imaging of renal artery stenosis: A multireader tricenter study.  J Am Soc Nephrol  2002; 13:158-169.

317. Michaely HJ, Schoenberg SO, Oesingmann N, et al: Renal artery stenosis: Functional assessment with dynamic MR perfusion measurements—feasibility study.  Radiology  2006; 238(2):586-596.

318. van den Dool SW, Wasser MN, de Fijter JW, et al: Functional renal volume: Quantitative analysis at gadolinium-enhanced MR angiography—feasibility study in healthy potential kidney donors.  Radiology  2005; 236:189-195.

319. Spuentrup E, Ruebben A, Stuber M, et al: Metallic renal artery MR imaging stent: Artifact-free lumen visualization with projection and standard renal MR angiography.  Radiology  2003; 227:897-902.

320. Nally Jr JV, Black HR: State-of-the-art review: Captopril renography—Pathophysiological considerations and clinical observations.  Semin Nucl Med  1992; 22:85-97.

321. Taylor A, Nally J, Aurell M, et al: Consensus report on ACE inhibitor renography for detecting renovascular hypertension. Radionuclides in Nephrourology Group. Consensus Group on ACEI Renography.  J Nucl Med  1996; 37:1876-1882.

322. Taylor Jr AT, Fletcher JW, Nally Jr JV, et al: Procedure guideline for diagnosis of renovascular hypertension. Society of Nuclear Medicine.  J Nucl Med  1998; 39:1297-1302.

323. Nally Jr JV, Chen C, Fine E, et al: Diagnostic criteria of renovascular hypertension with captopril renography: A consensus statement.  Am J Hypertens  1991; 4:749S-752S.

324. Fine EJ: Interventions in renal scintigraphy.  Semin Nucl Med  1999; 29:128-145.

325. Llach F, Papper S, Massey SG: The clinical spectrum of renal vein thrombosis: Acute and chronic.  Am J Med  1980; 69(6):819-827.

326. Witz M, Kantarovsky A, Baruch M, Shifrin EG: Renal vein occlusion: A review.  J Urol  1996; 155(4):1173-1179.

327. Llach F, Koffler A, Finck E, Massry SG: On the incidence of renal vein thrombosis in the nephrotic syndrome.  Arch Intern Med  1977; 137(3):333-336.

328. Gatewood OMB, Fishman EK, Burrow CR, et al: Renal vein thrombosis in patients with nephrotic syndrome: CT diagnosis.  Radiology  1986; 159:117-122.

329. Sebastia C, Quiroga S, Boye R, et al: Helical CT in renal transplantation: Normal findings and early and late complications.  RadioGraphics  2001; 21:1103-1117.

330. Brown ED, Chen MYM, Wolfman NT, et al: Complications of renal transplantation: Evaluation with US and radionuclide imaging.  RadioGraphics  2000; 20:607-622.

331. Letourneau JG, Day DL, Ascher NL, Castaneda-Zuniga WR: Perspective. Imaging of renal transplants.  Am J Roentgenol  1988; 150:833-838.

332. Kelcz F, Pazniak MA, Pirsch JD, Oberly TD: Pyramidal appearance and resistive index: Insensitive and nonspecific sonographic indicators of renal transplant rejection.  Am J Roentgenol  1990; 155:531-535.

333. Smith PA, Ratner LE, Lynch FC, et al: Role of CT angiography in the preoperative evaluation for laparoscopic nephrectomy.  RadioGraphics  1998; 18:589-601.

334. Holden A, Smith A, Dukes P, et al: Assessment of 100 live potential renal donors for laparoscopic nephrectomy with multi-detector row helical CT.  Radiology  2005; 237:973-980.

335. Rydberg J, Kopecky KK, Tann M, et al: Evaluation of prospective living renal donors for laparoscopic nephrectomy with multisection CT: The marriage of minimally invasive imaging with minimally invasive surgery.  RadioGraphics  2001; 21:S223-S236.

336. Kawamoto S, Montgomery R, Lawler LP, et al: Multi-detector row CT evaluation of living renal donors prior to laparoscopic nephrectomy.  Radiographics  2003; 24:1513-1514.

337. Hofmann LV, Smith PA, Kuszyk BS, et al: Original report. Three-dimensional helical CT angiography in renal transplant recipients: A new problem-solving tool.  Am J Roentgenol  1999; 173:1085-1089.

338. Pozniak MA, Balison DJ, Lee FT, et al: CT angiography of potential renal transplant donors.  RadioGraphics  1998; 18:565-587.

339. Kawamoto S, Lawler LP, Fishman EK: Evaluation of the renal venous system on late arterial and venous phase images with MDCT angiography in potential living laparoscopic renal donors.  Am J Roentgenol  2005; 184:539-545.

340. Sahani DV, Rastogi N, Greenfield AC, et al: Multi-detector row CT in evaluation of 94 living renal donors by readers with varied experience.  Radiology  2005; 235:905-910.

341. Rubin GD: Invited commentary. Helical CT of potential living renal donors: Toward a greater understanding.  RadioGraphics  1998; 18(3):601-604.

342. Hohenwalter MD, Skowlund CJ, Erickson SJ, et al: Renal transplant evaluation with MR angiography and MR imaging.  RadioGraphics  2001; 21:1505-1517.

343. Hussain SM, Kock MCJM, Ifzermans JNM, et al: MR imaging: A “one-stop shop” modality for preoperative evaluation of potential living kidney donors.  RadioGraphics  2003; 23:505-520.

344. Israel GM, Lee VS, Edye M, et al: Comprehensive MR imaging in the preoperative evaluation of living donor candidates for laparoscopic nephrectomy: Initial experience.  Radiology  2002; 225:427-432.

345. Van den Dool SW, Wasser MN, de Fijter JW, et al: Functional renal volume: Quantitative analysis at gadolinium-enhanced MR angiography—feasibility study in healthy potential kidney donors.  Radiology  2005; 236:189-195.

346. Akbar SA, Jafri ZH, Amendola MA, et al: Complications of renal transplantation.  RadioGraphics  2005; 25:1335-1356.

347. Allen KS, Jorkasky DK, Arger PH, et al: Renal allografts: Prospective analysis of Doppler sonography.  Radiology  1998; 169:371-376.

348. Grant EG, Perrella RR: Commentary. Wishing won't make it so: Duplex Doppler sonography in the evaluation of renal transplant dysfunction.  Am J Roentgenol  1990; 155:538-539.

349. Reuther G, Wanjura D, Bauer H: Acute renal vein thrombosis in renal allografts: Detection with duplex Doppler US.  Radiology  1989; 170:557-558.

350. Buckley AR, Cooperberg PL, Reeve CE, Magil AB: The distinction between acute renal transplant rejection and cyclosporine nephrotoxicity: Value of duplex sonography.  Am J Roentgenol  1987; 149:521-525.

351. Kaveggia LP, Perrella RR, Grant EG, et al: Duplex Doppler sonography in renal allografts: The significance of reversed flow in diastole.  Am J Roentgenol  1990; 155:295-298.

352. Voegeli DR, Crummy AB, McDermott JC, et al: Percutaneous management of the urological complications of renal transplantation.  RadioGraphics  1986; 6(6):1007-1022.

353. Patel NH, Jindal RM, Wilkin T, et al: Renal arterial stenosis in renal allografts: Retrospective study of predisposing factors and outcome after percutaneous transluminal angioplasty.  Radiology  2001; 219:663-667.

354. Vrachliotis TG, Vaswani KK, Davies EA, et al: Pictorial essay. CT findings in posttransplantation lymphoproliferative disorder of renal transplants.  Am J Roentgenol  2000; 175:183-188.

355. Sadowski EA, Fain SB, Alford SK, et al: Assessment of acute renal transplant rejection with blood oxygen level-dependent MR imaging: Initial experience.  Radiology  2005; 236:191-911.

356. Yang D, Ye Q, Williams DS, et al: Normal and transplanted rat kidneys: Diffusion MR imaging at 7 T.  Radiology  2004; 231:702-709.

357. Dubovsky EV, Russell CD, Erbas B: Radionuclide evaluation of renal transplants.  Semin Nucl Med  1995; 25(1):49-59.

358. Dunagin P, Alijani M, Atkins F, et al: Application of the kidney to aortic blood flow index to renal transplants.  Clin Nucl Med  1983; 8:360-364.

359. Lin E, Alavi A: Significance of early tubular extraction in the first minute of Tc-99m MAG3 renal transplant scintigraphy.  Clin Nucl Med  1998; 23(4):217-222.

360. Fortenbery EJ, Blue PW, Van Nostrand D, Anderson JH: Lymphocele: The spectrum of scintigraphic findings in lymphoceles associated with renal transplant.  J Nucl Med  1990; 31:1627-1631.

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