Harrisons Principles of Internal Medicine Self-Assessment and Board Review 18th Ed.

SECTION VII. Disorders of the Kidney and Urinary Tract


VII-1.  The answer is E. (Chap. 279) Ischemic acute renal failure has many potential etiologies. Microvascular disorders include increased vasoconstriction from endothelin and other mediators, decreased nitric oxide, prostaglandin- or bradykinin-mediated vasodilation, increased endothelial and vascular smooth muscle cell damage, and increased leukocyte adhesion. Tubular factors include cytoskeletal breakdown, loss of polarity, apoptosis and necrosis, desquamation of viable and necrotic cells, tubular obstruction, and backleak. Inflammatory and vasoactive mediators may affect both tubular and microvascular pathophysiologic mechanisms.

VII-2.  The answer is E. (Chap. 279) The risk for acute kidney injury is less well studied for abdominal procedures compared to cardiac surgery, but appears to be relatively comparable. Abdominal procedures, however, are not thought to be of particular risk compared with other major chest or orthopedic procedures. Common risk factors for postoperative acute kidney injury include underlying chronic kidney disease, older age, diabetes mellitus, congestive heart failure, and emergency procedures. Most commonly, postoperative acute kidney injury is multifactorial.

VII-3.  The answer is E. (Chap. 279) Iodinated contrast agents that are commonly used in cardiovascular and CT imaging are a major cause of acute kidney injury. Underlying mechanisms leading to kidney injury include transient tubular obstruction by contrast material, hypoxia in the other renal medulla due to alterations in renal microcirculation and occlusion of small vessels, and cytotoxic damage to the tubules directly or through the generation of free radicals by contrast material. Risk factors for contrast-associated nephropathy include diabetes mellitus, congestive heart failure, preexisting chronic kidney disease, and multiple myeloma–associated renal failure. Serum creatinine begins to rise at 24–48 hours and will peak at 3–5 days, usually with resolution within a week. Urinary sediment is bland, without casts. The fractional excretion of sodium is low in many cases, particularly early before tubular injury is extensive because of the microvascular source of injury.

VII-4.  The answer is B. (Chap. 279) Postrenal obstruction is an important and potentially reversible cause of acute kidney injury. Ultrasound evaluation of the kidneys classically demonstrates bilateral hydronephrosis, as unilateral obstruction is unlikely to cause kidney injury unless a single functioning kidney is present, chronic kidney disease preexists, or rarely, there is reflex vasospasm of the unobstructed kidney. Advanced cervical cancer with invasion into the urinary system or retroperitoneum is a common cause of obstructive uropathy. Thrombotic thrombocytopenic purpura (TTP), disseminated gonococcus with sepsis, and pyelonephritis are intrinsic causes of acute kidney failure and will not cause bilateral hydronephrosis.

VII-5.  The answer is B. (Chap. 279) Cholesterol emboli are an important cause of acute kidney injury in patients who have undergone cardiac procedures that may disrupt aortic atherosclerotic disease and shower cholesterol emboli. Livedo reticularis is a common finding on physical examination and peripheral blood eosinophilia may be present. When found, eosinophiluria is highly suggestive. The other major cause of eosinophiluria is acute interstitial nephritis. White blood cell casts suggest interstitial nephritis, pyelonephritis, glomerulonephritis, or malignant infiltration of the kidney; calcium oxalate crystals are found in ethylene glycol intoxication; and granular casts are suggestive of acute ischemic kidney injury (acute tubular necrosis), glomerulonephritis, vasculitis, or tubulointerstitial nephritis.

VII-6.  The answer is E. (Chap. 279) Multiple studies have demonstrated that acute kidney injury is an independent poor prognostic indicator in critically ill patents with multiple medical conditions. Unfortunately, care of critically ill patients with acute kidney injury is supportive, as no specific therapy has been shown to improve outcomes. Agents that have specifically been shown to have no benefit in the treatment of acute tubular injury include atrial natriuretic peptide, low-dose dopamine, endothelin antagonists, loop diuretics, calcium channel blockers, α-adrenergic receptor blockers, prostaglandin analogs, antioxidants, insulin-like growth factor, and antibodies against leukocyte adhesion molecules. Volume repletion is critical to ensure adequate perfusion, and diuretics are only indicated in patients with replete fluid status and low urinary flow rates.

VII-7.  The answer is A. (Chap. 279) Nonsteroidal anti-inflammatory drugs (NSAIDs) do not alter glomerular filtration rate in normal individuals. However, in states of mild to moderate hypoperfusion (as in prerenal azotemia) or in the presence of chronic kidney disease, glomerular perfusion and filtration fraction are preserved through several compensatory mechanisms. In response to a reduction in perfusion pressures, stretch receptors in afferent arterioles trigger a cascade of events that lead to afferent arteriolar dilatation and efferent arteriolar vasoconstriction, thereby preserving glomerular filtration fraction. These mechanisms are partly mediated by the vasodilators prostaglandin E2and prostacyclin. NSAIDs can impair the kidney’s ability to compensate for a low perfusion pressure by interfering with local prostaglandin synthesis and inhibiting these protective responses. Ureteral obstruction is not the mechanism by which NSAIDs impair renal function in this scenario. NSAIDs are not known to be proximal tubule toxins.

VII-8.  The answer is E. (Chap. 279) Radiocontrast agents cause renal injury through intrarenal vasoconstriction and the generation of oxygen radicals, causing acute tubular necrosis. These medications cause an acute decrease in renal blood flow and glomerular filtration rate. Patients with chronic kidney disease, diabetes mellitus, heart failure, multiple myeloma, and volume depletion are at the highest risk of contrast nephropathy. It is clear that hydration with normal saline is an effective measure to prevent contrast nephropathy. Of the other measures mentioned here, only sodium bicarbonate or N-acetylcysteine could be recommended for clinical use to reduce the risk of contrast nephropathy. Dopamine has been proven an ineffective agent to prevent contrast nephropathy. Fenoldopam, a D1-receptor agonist, has been tested in several clinical trials and does not appear to reduce the incidence of contrast nephropathy. Although several small clinical studies have suggested a clinical benefit to the use of N-acetylcysteine, a meta-analysis has been inconclusive, and the medication should be administered well in advance of the procedure. Sodium bicarbonate begun within 1 hour of the procedure has shown a significant benefit in a single-center, randomized controlled trial. Due to the time limitations, and based on the evidence, only sodium bicarbonate would be helpful in this patient.

VII-9.  The answer is C. (Chap. 280) Chronic kidney disease is classified by glomerular filtration rate. In stage 0 patients, GFR is greater than 90 mL/min per 1.73 m2, stage 2 GFR is 60–89 mL/min per 1.73 m2, stage 3 GFR is 30–59 mL/min per 1.73 m2, and stage 4 GFR is 15–29 mL/min per 1.73 m2. Stage 5 GFR is less than 15 mL/min per 1.73 m2.

VII-10. The answer is A. (Chap. 280) The leading cause of morbidity and mortality in patients with chronic kidney disease regardless of stage is cardiovascular disease. The presence of chronic kidney disease is a major risk factor for ischemic heart disease; in addition to traditional cardiovascular risk factors, patients with chronic kidney disease have additional risk factors including anemia, hyperphosphatemia, hyperparathyroidism, sleep apnea, and systemic inflammation. Left ventricular hypertrophy and dilated cardiomyopathy are also frequently present in those with chronic kidney disease and are strongly associated with cardiovascular morbidity and mortality.

VII-11. The answer is B. (Chap. 280) Anemia is a common consequence of chronic kidney disease and may be multifactorial, with etiologies including relative erythropoietin deficiency, iron deficiency, chronic inflammation, diminished red cell survival, and bleeding diathesis. Several trials of erythropoietin supplementation in patients with chronic kidney disease have failed to show improved cardiovascular outcomes with this therapy. Indeed, these trials have shown a higher incidence of thromboembolic events, stroke in Type 2 diabetics, and potentially faster progression to need for dialysis. Because of these concerning findings, erythropoietin use has been altered from prior recommendations, and current practice is to target a hemoglobin concentration of 100–115 g/L.

VII-12. The answer is B. (Chap. 281) The commonly accepted criteria for initiating patients on maintenance dialysis include the presence of uremic symptoms, the presence of hyper-kalemia unresponsive to conservative management, persistent extracellular volume expansion despite diuretics, acidosis refractory to medical therapy, bleeding diathesis, or a creatinine clearance or estimated GFR below 10 mL/min per 1.73m2. BUN or creatinine values alone are inadequate to initiate dialysis.

VII-13. The answer is E. (Chap. 281) Hypotension is the most common complication of hemodialysis. There are many potential etiologies of hypotension including antihypertensive use, excessive ultrafiltration, impaired vasoactive or autonomic responses, impaired cardiac reserve, and osmolar shifts. Less common causes include dialyzer reactions and high-output heart failure related to large arteriovenous (AV) fistulae. Manipulation of buffer for dialysate, alterations of timing of ultrafiltration, and midodrine may be used to improve hemodynamic tolerance to hemodialysis. Patients with unexpected or new hypotension during stable dialysis should also be evaluated for graft infection and bacteremia.

VII-14. The answer is E. (Chap. 281) The major complication of peritoneal dialysis therapy is peritonitis, though other complications include catheter-associated non-peritonitis infections, weight gain, metabolic derangements, and residual uremia. Peritonitis is usually a result from a failure of sterile technique during the exchange procedure. Transvisceral infection from the bowel is much less common. Because of the high dextrose used in dialysate, the environment is conducive for the development of bacterial infection. This can be diagnosed by the presence of more than 100/mm3 leukocytes with more than 50% polymorphonuclear cells on microscopy. Cloudy dialysate and abdominal pain are the most common symptoms. The most commonly isolated bacteria are skin flora such as Staphylococcus. Gram-negative organisms, fungi, and mycobacteria have also been described. A recent Cochrane review (Wiggins KJ et al: Treatment for peritoneal dialysis-associated peritonitis. Cochrane Database of Systematic Reviews 2008, Issue 1. Art. No.: CD005284. DOI: 10.1002/14651858.CD005284.pub2) concluded that intraperitoneal administration of antibiotics was more effective than intravenous administration, and that adjunctive treatment with urokinase or peritoneal lavage offers no advantage. Intraperito-neal vancomycin is common initial empiric therapy.

VII-15. The answer is C. (Chap. 281) The most common cause of mortality in patients with end-stage renal disease is cardiovascular disease (stroke and myocardial infarction). Although the underlying mechanisms driving this association are under active investigation, the shared risk factors of diabetes, hypertension, and dyslipidemia in addition to specific risks such as increased inflammation, hyperhomocysteinemia, anemia, and altered vascular function are thought to play an important role. Inefficient or inadequate dialysis is a risk for patients with difficult vascular access or poor adherence to therapy. Patients receiving hemodialysis are at risk and often develop neurologic, hematologic, and infectious complications. Nevertheless, the biggest risk to survival in these patients is also the most common cause of death in the general population.

VII-16. The answer is B. (Chap. 281) Although the dose is currently defined as a derivation of the fractional urea clearance, factors that are also important include patient size, residual kidney function, dietary protein intake, comorbid conditions, and the degree of anabolism/catabolism. The efficiency of dialysis depends on the counter-current flow rate of the dialysate. The number of hours/sessions prescribed for a patient is derived from the dialysis dose and is individualized.

VII-17. The answer is A. (Chap. 281) The potassium concentration of dialysate is usually 2.5 meq/L but may be varied depending on the predialysis serum potassium. This patient may need a lower dialysate potassium concentration. Sodium modeling is an adjustment of the dialysate sodium that may lessen the incidence of hypotension at the end of a dialysis session. Aldosterone defects, if present, are not likely to play a role in this patient since his kidneys are not being perfused. Therefore, nephrectomy is not likely to control his potassium. Similarly, since the patient is likely anuric, there is no efficacy in utilizing loop diuretics to effect kaluresis. This patient has no approved indications for implantation of a defibrillator.

VII-18. The answer is D. (Chap. 282) Both deceased and living donor kidney transplantations are highly successful. When compared to hemodialysis there are substantial cost-benefit advantages to individuals and society related to decreased morbidity, subsequent hospitalizations, and mortality. When first-degree relatives are donors, the graft survival rates are higher than those of deceased donors by 5–7% at 1 year. This difference persists for up to 10 years. There are few reported complications for donors, particularly in the absence of hypertension or diabetes mellitus. For deceased donors, older age, the presence of preexisting renal damage, or prolonged ischemia decreases the longevity of the graft.

VII-19. The answer is B. (Chap. 283) There are a wide variety of diseases that can cause glomerular injury to the kidney, ranging from genetic conditions such as TRPC6 mutation causing cation channel dysfunction and associated focal segmental glomerulosclerosis to glomerular stress from systemic hypertension and/or diabetes mellitus. Inflammatory disease such as lupus nephritis, Wegener’s granulomatosis, and poststreptococcal glomerulonephritis may also cause glomerular disease. Fanconi’s syndrome is a classic disease of tubular dysfunction with associated aminoaciduria, type 2 renal tubular acidosis, and rickets, not glomerular disease.

VII-20. The answer is C. (Chap. 283) The hallmark of glomerular renal disease is microscopic hematuria and proteinuria. IgA nephropathy and sickle cell disease are the exception to this when gross hematuria may be present. Proteinuria may be heavy (>3 g/24 hours) or lower quantity with microalbuminuria (30–300 mg/24 hours) depending on the underlying disease or site of the immune lesion. Patients with post-streptococcal glomerulonephritis often have pyuria, but cultures are not expected to be positive as the infection is usually skin or mucosal, and it is the immune reaction that drives the renal lesion.

VII-21. The answer is B. (Chap. 283) The characteristic pattern of focal (not all glomeruli) and segmental (not the entire glomerulus) glomerular scarring is shown. The history and laboratory features are also consistent with this lesion: some associated hypertension, diminution in creatinine clearance, and a relatively inactive urine sediment. The “nephropathy of obesity” may be associated with this lesion secondary to hyperfiltration; this condition may be more likely to occur in obese patients with hypoxemia, obstructive sleep apnea, and right-sided heart failure. Hypertensive nephrosclerosis exhibits more prominent vascular changes and patchy, ischemic, totally sclerosed glomeruli. In addition, nephrosclerosis seldom is associated with nephrotic-range proteinuria. Minimal-change disease usually is associated with symptomatic edema and normal-appearing glomeruli, as demonstrated on light microscopy. This patient’s presentation is consistent with that of membranous nephropathy, but the biopsy is not. With membranous glomerular nephritis all glomeruli are uniformly involved with subepithelial dense deposits. There are no features of crescentic glomerulonephritis present.

VII-22. The answer is E. (Chap. 284) Autosomal polycystic kidney disease is a common genetic disorder accounting for up to 4% of end-stage renal disease cases in the United States. Although the most common manifestations of this condition are renal cysts, hematuria, urinary tract infection, and occasionally nephrolithiasis, there are several common extra-renal manifestations including intracranial aneurysm, aortic root and annulus dilatation, valvular heart disease including aortic regurgitation and mitral valve prolapse, hepatic cysts, hernias, and colonic diverticulae with a high propensity to perforate.

VII-23. The answer is C. (Chap. 284) The patient presents with hypokalemia and hypochloremic metabolic alkalosis in the absence of hypertension. This is most commonly due to surreptitious vomiting or diuretic abuse, but in this case the urine diuretic screen was negative. In patients with surreptitious vomiting, urine chloride levels are low to preserve intravascular volume and this was not present in this patient. Those with Bartter’s syndrome and Gitelman’s syndrome have hypokalemia and hypochloremic metabolic alkalosis with inappropriately elevated urine chloride levels. Gitelman’s syndrome is less severe and presents later in life than Bartter’s, which is commonly found in childhood due to failure to thrive. Additionally, those with Gitelman’s syndrome have more prominent fatigue and muscle cramping. Most forms of Bartter’s syndrome also include associated hypomagnesemia and hypocalciuria. Those with type 1 pseudohypoaldosteronism have severe renal salt wasting and hyperkalemia. Liddle’s syndrome presents with apparent aldosterone excess with severe hypertension, hypokalemia, and metabolic alkalosis.

VII-24. The answer is E. (Chap. 284) Patients with autosomal dominant polycystic kidney disease have a two- to fourfold increased risk of subarachnoid or cerebral hemorrhage compared to the general population. Hemorrhage tends to occur before age 50 in patients with a family history of intracranial hemorrhage, patients with a personal history of intracranial hemorrhage, aneurysms larger than 10 mm, or patients with uncontrolled hypertension.

VII-25. The answer is A. (Chap. 284) This patient has a normal anion gap metabolic acidosis (anion gap = 12). The calculated urine anion gap (Na+ + K+ − Cl) is +3; thus the acidosis is unlikely to be due to gastrointestinal bicarbonate loss. In this patient the diagnosis is type I renal tubular acidosis, or distal RTA. This is a disorder in which the distal nephron does not lower pH normally. It is associated with a urine pH greater than 5.5, hypokalemia, and lack of bicarbonaturia. This condition may be associated with calcium phosphate stones and nephrocalcinosis. Type II RTA, or proximal RTA, includes a pH less than 5.5, hypokalemia, a positive urine anion gap, bicarbonaturia, hypophosphatemia, and hyper-calciuria. This condition results from the defective resorption of bicarbonate. Type III RTA is rare and most commonly is seen in children. Type IV RTA is also referred to as hyperkalemic distal RTA. Hyporeninemic hypoaldosteronism is the most common cause of type IV RTA and is usually associated with diabetic nephropathy.

VII-26. The answer is D. (Chap. 284) In any patient with hypokalemia the use of diuretics must be excluded. This patient has multiple warning signs for the use of agents to alter her weight, including her age, gender, and participation in competitive sports. Her BMI is low, and the oral examination may suggest chronic vomiting. Chronic vomiting may be associated with a low urine chloride level. Once diuretic use and vomiting are excluded, the differential diagnosis of hypokalemia and metabolic alkalosis includes magnesium deficiency, Liddle’s syndrome, Bartter’s syndrome, and Gitelman’s syndrome. Liddle’s syndrome is associated with hypertension and undetectable aldosterone and renin levels. It is a rare autosomal-dominant disorder. Classic Bartter’s syndrome has a presentation similar to that of this patient. It may also include polyuria and nocturia because of hypokalemia-induced diabetes insipidus. Gitelman’s syndrome can be distinguished from Bartter’s syndrome by hypomagnesemia and hypocalciuria.

VII-27. The answer is A. (Chap. 285) Acute interstitial nephritis is a common cause of both acute and chronic kidney dysfunction. Many causes of interstitial nephritis are successfully treated with glucocorticoids with improved rates of long-term renal recovery including Sjögren’s syndrome, sarcoidosis, systemic lupus erythematosus, adults with tubulointerstitial nephritis with uveitis, and idiopathic or other granulomatous interstitial nephritis. In patients with gradually progressive disease or fibrosis on biopsy, the benefit is less clear. Additionally, allergic interstitial nephritis recovery may be accelerated with glucocorticoid therapy, but long-term renal recovery has not been proven to improve. Postinfectious interstitial nephritis has been associated with many bacterial and viral pathogens, but generally resolves with treatment of the underlying condition.

VII-28. The answer is E. (Chap. 285) Allergic interstitial nephritis is a common cause of unexplained acute renal failure. This is generally a clinical diagnosis with acute renal failure in the context of exposure to a potential offending agent (often NSAIDs, antibiotics, anticonvulsants, or proton pump inhibitors) and improvement in renal function with withdrawal of the agent. Peripheral blood eosinophilia supports the diagnosis, but is rarely found. Urine microscopy often shows white blood cell casts and hematuria, but these are not specific findings. Urine eosinophils are neither sensitive nor specific for allergic interstitial nephritis. A renal biopsy is generally not required but may show extensive tubulointerstitial infiltration of white cells including eosinophils.

VII-29. The answer is A. (Chap. 286) The patient presents with the classic pentad for thrombotic thrombocytopenic purpura (TTP), including fever, neurologic findings, renal failure, hemolytic anemia, and thrombocytopenia. This condition is more common in women than men, and in black than white patients, and may be triggered by a number of factors including pregnancy, infection, surgery, and pancreatitis. Several drugs have been implicated in the pathogenesis of TTP such as immunosuppressive agents, chemo-therapeutic agents, and antiplatelet drugs. TTP may be differentiated from hemolytic uremic syndrome (HUS) by the demographics, with HUS typically affecting young children and TTP being more common in middle-aged persons. Additionally, HUS is generally triggered by a diarrheal illness, which is much less common in TTP. On a molecular level, the metalloprotease ADAMTS13 specific for von Willebrand factor (vWF) is generally low if not absent in activity in TTP. The development of HUS is likely driven by bacterial toxins such as shiga toxin or shiga-like toxin, often from E. coli 0157:H7. Because TTP is associated with low protein levels that may be driven by autoantibodies, plasma exchange serves the dual purpose of removing the aberrant antibody and repleting protein levels. With appropriate therapy, 1-month mortality is approximately 20%. Untreated mortality nears 90%, primarily from microvascular thrombosis and multiorgan failure.

VII-30. The answer is C. (Chap. 286) Renal vein thrombosis occurs in 10–15% of patients with nephrotic syndrome accompanying membranous glomerulopathy and oncologic disease. The clinical manifestations can be variable but may be characterized by fever, lumbar tenderness, leukocytosis, and hematuria. Magnetic resonance venography is the most sensitive and specific noninvasive form of imaging to make the diagnosis of renal vein thrombosis. Ultrasound with Doppler is operator dependent and therefore may be less sensitive. Contrast venography is the gold standard for diagnosis, but it exposes the patient to a more invasive procedure and contrast load. Nuclear medicine screening is not performed to make this diagnosis.

VII-31. The answer is A. (Chap. 287) Calcium stones account for 75–85% of all kidney stones. Although they are most commonly caused by idiopathic hypercalciuria, hypocitraturia, hyperuricosuria, and primary hyperparathyroidism are also causes. Uric acid stones are the next most common stone, followed by cysteine and struvite. Oxalic acid does not form stones without complexing with a positive cation, such as calcium. Struvite stones are precipitated by bacterial infections, such as Proteus, that promote conversion of urea to ammonium and raise urinary pH. General management for calcium stones includes increasing consumption of water, low protein, and low calcium. If this is ineffective, thiazide diuretics may be used.

VII-32. The answer is D. (Chap. 289) Urinary tract obstruction is an important and potentially reversible cause of kidney failure. This patient is at risk for urinary obstruction based on her history of colon cancer. Although recent NSAID use may be contributing to the rapidity of her kidney damage, routine dosing is less likely to cause acute kidney injury in the absence of preexisting renal dysfunction. Ultrasound of the kidneys is the best screening test for obstruction. Hydroureter and/or hydronephrosis may be found and suggest the presence of obstruction. Although obstruction may be unilateral, it rarely causes clinically significant renal failure in the absence of underlying renal disease. CT of the abdomen is useful after ultrasound to evaluate the site and etiology of obstruction. Post-void residual is useful if functional causes of obstruction are suspected, such as urinary retention. After the obstruction site is located, retrograde urography with stent placement may be indicated, but only after defining the presence or absence of obstruction.

VII-33 and VII-34. The answers are E and D, respectively. (Chap. 289) The patient has relief of recent urinary obstruction and is now making an inappropriately large amount of urine. This is likely due to postobstructive diuresis, which results from release of obstruction, increase in GFR over the course of days, decreased tubule pressure, and increased solute load per nephron, resulting in increased urine output. Decreased medullary osmolarity is a feature of chronic obstruction and persistent obstruction. The patient has not had recent head trauma or neurosurgical procedure and is unlikely to have cerebral salt wasting. Increased activation of the renin-angiotensin-aldosterone system is associated with chronic, unrelieved obstruction. Patients with postobstructive diuresis are at risk for volume depletion with possible development of prerenal azotemia and resultant acute kidney injury, as well as electrolyte imbalance, particularly due to losses of Na, K, PO4, Mg, and free water. Erythrocytosis may be seen in patients with obstruction, but is a rare feature and is not associated with postobstructive diuresis. Systemic hypotension is more common than hypertension due to volume depletion.

VII-35. The answer is C. (Chap. 289) In acute urinary tract obstruction, pain is due to distention of the collecting system or renal capsule. Acutely, there is a compensatory increase in renal blood flow when kidney function is impaired by obstruction, which further exacerbates capsular stretch. Eventually, vasodilatory prostaglandins act to preserve renal function when glomerular filtration rate has decreased. Medullary blood flow decreases as the pressure of the obstruction further inhibits the renal parenchyma from perfusing; however, the ensuing chronic renal destruction may occur without substantial pain. When an obstruction has been relieved, there is a postobstructive diuresis that is mediated by relief of tubular pressure, increased solute load (per nephron), and natriuretic factors. There can be an extreme amount of diuresis, but this is not painful.

VII-36. The answer is D. (Chap. 289) The level of obstruction is important when considering urinary tract obstruction. Bilateral hydronephrosis and hydroureter suggest either a systemic process or mechanical obstruction at or below the level of the uretero-vesical junctions. While retroperitoneal fibrosis can cause such a picture, it is most common among middle-aged men. In patients of reproductive age, genital tract infections can cause meatal stenosis if left untreated or if infections are recurrent. Retroperitoneal lymphomas can cause bilateral hydroureter, as can more distal obstructions like phimosis. In the developing world, one may also consider schistosomiasis and genitourinary tuberculosis.