Marc D. Squillante
Distinction between community- and hospital-acquired acute renal failure (ARF) is important for differential diagnosis, treatment, and outcome.
Prerenal ARF is the most common community-acquired cause, accounting for 70% of patients. Majority of cases are due to volume depletion. Up to 90% of patients presenting to an ED have a potentially reversible cause.
Intrinsic renal causes, particularly acute tubular necrosis (ATN), are the most common etiology for hospital-acquired ARF, accounting for 70% of patients. Common in ICU and multi-organ failure patients.
Postrenal causes account for 10% of patient in both community- and hospital-acquired ARF.
Mortality rates depend on severity and cause of renal failure. Most adult ARF deaths are due to sepsis and cardiopulmonary failure. Hospital-acquired ARF has a higher mortality.
The RIFLE classification has established three grades of renal compromise of increasing severity (Risk, Injury, and Failure), and two outcome measures (Loss, and End-stage renal disease), which correlate with prognosis. Grading renal risk, injury, failure can be accomplished using either serum creatinine/glomerular filtration rate (GFR) criteria, or by urine output criteria over 6 to 24 hours.
Use of the serum creatinine change from baseline is the most useful for the emergency physician seeing the patient during a small window of time in the ED: renal risk = serum creatinine increased 1.5 times baseline; renal injury = serum creatinine increased 2 times baseline; renal failure = serum creatinine increased 3 times baseline or creatinine greater than 4.0 milligrams/dL and acute increase over 0.5 milligram/dL.
Mortality from ARF has been stable for decades, in spite of use of dialysis.
Pediatric ARF has a different set of etiologies, and mortality averages 25%.
Decreases in renal blood flow (RBF) are the final common pathway for most causes of ARF.
Tubular and glomerular functions are maintained in prerenal failure, but GFR is depressed by compromised renal perfusion.
Prerenal failure is produced by conditions that decrease renal perfusion (Table 52-1), and is the most common cause of community-acquired ARF (70% of cases). It is a common precursor to ischemic and nephrotoxic causes of intrinsic renal failure as well.
Ischemic ARF (traditionally known as ATN, but now called acute kidney injury [AKI]), is the most common cause of intrinsic renal failure. The renal parenchyma suffers ischemic injury due to significant decreases in renal perfusion. This is the most common cause of hospital-acquired ARF.
Intrinsic renal failure occurs with diseases of the glomerulus, interstitium, or tubules, associated with the release of renal vasoconstrictors.
The etiologies of intrinsic renal failure are subdivided anatomically into small-vessel disease, primary glomerular disease, and tubular and interstitial diseases (Table 52-1).
Nephrotoxins are the second most common cause of ATN, accounting for approximately 25%.
ARF has a different spectrum in the pediatric population: a higher incidence of intrinsic renal causes for ARF (45%) secondary to diseases such as glomeru-lonephritis and hemolytic-uremic syndrome.
Postobstructive ARF increases tubular pressure, which decreases filtration. It has a significantly higher incidence in selected populations (such as elderly men).
Restoring RBF is key to recovery from ARF.
Replacement of circulating volume is critical in prerenal ARF.
Treatment of the underlying cause of intrinsic ARF (toxin clearance, therapy for glomerular diseases) helps restore RBF.
Vasoconstriction and tubular pressure decrease with relief of postrenal obstruction.
TABLE 52-1 Causes of Renal Failure
Deterioration in renal function leads to excessive accumulation of nitrogenous waste products in the serum. Patients usually have signs and symptoms of their underlying causative disorder but eventually develop stigmata of renal failure.
Volume overload, hypertension, pulmonary edema, mental status changes or neurologic symptoms, nausea and vomiting, bone and joint problems, anemia, and increased susceptibility to infection (a leading cause of death) can occur as patients develop more chronic uremia.
DIAGNOSIS AND DIFFERENTIAL
History and physical examination usually provide clues to etiology. Signs and symptoms of the underlying causative disorder (Table 52-1) should be vigorously sought.
Physical examination should assess vital signs, volume status, establish urinary tract patency and output, and search for signs of chemical intoxication, drug usage, muscle damage, infections, or associated systemic diseases.
Diagnostic studies include urinalysis (see Table 52-2), blood urea nitrogen and creatinine levels, serum electrolytes, urinary sodium and creatinine, and urinary osmolality. Analysis of these tests allows most patients to be categorized as prerenal, renal, or post-renal. Fractional excretion of sodium can be calculated to help in this categorization (see Table 52-3).
Normal urinary sediment may be seen in prerenal and postrenal failure, hemolytic-uremic syndrome, and thrombotic thrombocytopenic purpura. The presence of albumin may indicate glomerulonephritis or malignant hypertension.
Granular casts are seen in ATN. Albumin and red blood cell casts are found in glomerulonephritis, malignant hypertension, and autoimmune disease. White blood cell casts are seen in interstitial nephritis and pyelonephritis. Crystals can be present with renal calculi and certain drugs (sulfas, ethylene glycol, and radiocontrast agents).
Renal ultrasound is the radiologic procedure of choice in most patients with ARF when upper tract obstruction and hydronephrosis is suspected. Color flow Doppler can assess renal perfusion and diagnose large vessel causes of renal failure. Bedside sonography can quickly diagnose some treatable causes and give guidance for fluid resuscitation; inspiratory collapse of the intrahepatic IVC can give a good measure of volume status and fluid responsiveness (see Figs. 52-1A and 52–1B, and 52–2A and 52–2B).
Prerenal failure is produced by conditions that decrease renal perfusion (see Table 52-1) and is the most common cause of community-acquired ARF (∼70% of cases). It also is a common precursor to ischemic and nephrotoxic causes of intrinsic renal failure.
Intrinsic renal failure has vascular and ischemic etiologies; glomerular and tubulointerstitial diseases are also causative. (Ischemic ARF—traditionally known as ATN—is now called AKI.)
ATN due to severe and prolonged prerenal etiologies causes most cases of intrinsic renal failure; ATN is also the most common cause of hospital-acquired ARF.
Nephrotoxins are the second most common cause of ATN.
Postrenal azotemia occurs primarily in elderly men with high-grade prostatic obstruction. Lesions of the external genitalia (ie, strictures) are also common causes. Significant permanent loss of renal function occurs over 10 to 14 days with complete obstruction, and worsens with associated UTI.
TABLE 52-2 Urine Findings in Different Types of Renal Failure
TABLE 52-3 Laboratory Studies Aiding in the Differential Diagnosis of Acute Renal Failure
FIG. 52-1 A. US of normal kidney and kidney showing hydronephrosis. Normal kidney, capsule margin at arrows. B. Hydronephrosis as would be expected in obstructive uropa-thy; the dilated kidney fills the majority of the screen, capsule at arrows. (Courtesy of Michael B. Stone, MD, RDMS.)
FIG. 52-2 US of the inferior vena cava. A. Plethoric inferior vena cava (arrows) as might be expected in volume overload; there is very little respiratory variation. B. An almost fully collapsed inferior vena cava at inspiration (arrows) and expiration (arrowheads) as might be expected in prerenal acute renal failure. (Courtesy of Michael B. Stone, MD, RDMS.)
EMERGENCY DEPARTMENT CARE AND DISPOSITION
ED goals in the initial care of patients with ARF focus on treating the underlying cause and correcting fluid and electrolyte derangements. Efforts should be made to prevent further renal damage and provide supportive care until renal function has recovered (see Chap. 6 for treatment of electrolyte and acid-base disorders).
Effective intravascular volume should be restored with isotonic fluids (normal saline or lactated Ringer solution) at a rapid rate in appropriate patients; volume resuscitation is the first priority.
If cardiac failure is causing prerenal azotemia, cardiac output should be optimized to improve renal perfusion, and reduction in intravascular volume (ie, with diuretics) may be appropriate.
RENAL FAILURE (INTRINSIC)
Adequate circulating volume must be restored first; hypovolemia potentiates and exacerbates all forms of ARF.
Ischemia or nephrotoxic agents are the most common causes of intrinsic ARF. History physical examination, and baseline laboratory tests should provide clues to the diagnosis. Nephrotoxic agents (drugs and radiocontrast) should be avoided.
Low-dose dopamine (1–5 micrograms/kg/min) may improve RBF and urine output, but it does not lower mortality rates or improve recovery.
Renally excreted drugs (digoxin, magnesium, sedatives, and narcotics) should be used with caution because therapeutic doses may accumulate to excess and cause serious side effects. Fluid restriction may be required. Interventions useful in the prevention of radiocontrast nephropathy include acetylcysteine, fenoldopam, and crystalloid infusions.
Appropriate urinary drainage should be established; the exact procedure depends on the level of obstruction.
A Foley catheter should be placed to relieve obstruction caused by prostatic hypertrophy. There is no support for the practice of intermittent catheter clamping to prevent hypotension and hematuria; urine should be completely and rapidly drained.
Percutaneous nephrostomy may be required for ure-teral occlusion until definitive surgery to correct the obstruction can take place once the patient is stabilized.
For the acutely anuric patient, obstruction is the major consideration. If no urine is obtained on initial bladder catheterization, emergency urologic consultation should be considered.
With chronic urinary retention, postobstructive diuresis may occur due to osmotic diuresis or tubular dysfunction. Patients may become suddenly hypovo-lemic and hypotensive. Urine output must be closely monitored, with appropriate fluid replacement.
If treatment of the underlying cause fails to improve renal function, hemodialysis or peritoneal dialysis should be considered. The nephrology consultant usually makes decisions about dialysis (see Table 52-4).
Dialysis often is initiated when the blood urea nitrogen is greater than 100 milligrams/dL or serum creatinine is greater than 10 milligrams/dL.
Patients with complications of ARF such as cardiac instability (due to metabolic acidosis and hyperkalemia), intractable volume overload, hyperkalemia, and uremia (ie, encephalopathy, pericarditis, and bleeding diathesis) not easily corrected by other measures should be considered for emergency dialysis. However, morality in ARF has changed little since the advent of dialysis.
TABLE 52-4 Indications for Emergent Dialysis
Uncontrolled hyperkalemia (K+ >6.5 mmol/L or rising)
Intractable fluid overload in association with persistent hypoxia, or lack of response to conservative measures
Progressive uremic/metabolic encephalopathy; asterixis, seizures
Serum sodium level <115 or >165 mEq/L
Severe metabolic acidosis resistant to sodium bicarbonate, or cases in which repeat dosing of sodium bicarbonate is contraindicated
Life-threatening poisoning with a dialyzable drug, such as lithium, aspirin, methanol, ethylene glycol, or theophylline
Bleeding dyscrasia secondary to uremia
Excessive BUN and creatinine levels: trigger levels are arbitrary; it is generally advisable to keep BUN level <100 milligrams/dL, but each patient should be evaluated individually
Abbreviation: BUN = blood urea nitrogen.
Patients with new-onset ARF usually require hospital admission, often to an intensive care unit. Transferring patients to another institution should be considered if nephrology consultation and dialysis facilities are not available.
For further reading in Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 7th ed., see Chapter 91, “Acute Renal Failure,” by Richard Sineirt and Peter R. Peacock, Jr.