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ACUTE RENAL FAILURE
Method of

The Urogenital Tract

Kevin Schroeder, MD

CURRENT DIAGNOSIS
• Prerenal azotemia may be associated with a BUN-to-creatinine ratio >20:1 and a FENa 75

Mean blood pressure (in humans)

50 < too much flow > 25 Autoregulatory range 0 0 30 60 90 120 150 180 Mean blood pressure (mm Hg) 210

and mortality when these diseases are untreated, RPGN should be considered a medical emergency, with prompt attempts to diagnose and treat. It is important to recognize that whereas diseases that primarily manifest as the nephritic syndrome commonly cause ARF, entities associated more with a nephrotic-syndrome picture— including membranous disease, minimal change disease, or focal sclerosis—can certainly produce ARF as well. This usually occurs in the setting of massive nephrotic-range proteinuria (10–20 g/24 hours) and associated marked hypoalbuminemia.

Acute Tubular Necrosis
Acute tublar necrosis (ATN) accounts for fully 50% of ARF among hospitalized patients; depending on the scenario, this figure can rise to as much as 75%. ATN has three common causes: ischemic, toxic, and septic. ATN has been described by its phases: Injury, during which time the insult causes direct damage to the tubules, is manifested as a progressive increase in the serum creatinine and possibly the development of oliguria. In the plateau phase, the creatinine, urinary output, and volume status are relatively stable. Recovery is marked by a spontaneous decline in serum creatinine and increase in urinary output, perhaps even into a polyuric range. The time course of ATN from injury to recovery is variable. Depending on the severity of the injury and the preexistence of renal disease, ATN can reverse within 1 to 3 weeks, although a small percentage of patients with ATN remain dialysis dependent after months. ATN is typically associated with a loss of urinary concentration, elevated urinary sodium excretion, and an elevated FENa of greater than 2%. The BUN and creatinine tend to rise proportionally. The urinary sediment can reveal tubular epithelial cell casts that have a coarsely granular or muddy brown appearance. Ischemic ATN typically occurs during periods of prolonged hypotension and represents an evolution of prerenal azotemia. Ischemic ATN is commonly observed to varying degrees after cardiovascular and major orthopedic or trauma surgery. Careful attention must be paid to urine output and volume status. Highdose diuretics may be employed to avoid pulmonary edema, and if a suboptimal response is seen, the dosage should be doubled after the first dose. Patients who rapidly become oliguric have a high mortality rate, which is unaffected by diuretics and can therefore require early initiation of dialysis. Specific risk factors for developing ischemic ATN in the postoperative setting include advanced age (older than 70 years), preexisting CKD, diabetes, emergent surgery, preexisting vascular disease, and the need for valvular, particularly aortic valve, heart surgery in addition to bypass grafting. The degree and duration of intraoperative hypotension as well as time spent on cardiopulmonary bypass can also play roles. Toxic ATN is proximal tubular cell death as a consequence of drugs or other endogenous chemicals. Drugs that classically cause toxic ATN include aminoglycosides, amphotericin B (Fungizone), radiocontrast, platinum-based chemotherapy, and NSAIDs. Endogenous chemicals known to cause toxic ATN include uric acid, myoglobin, and heme. Clinically, it is worthwhile noting that although the onset of ATN after a single dose of NSAID or iodinated radiocontrast material may be rapid (24–72 hours) especially in volume-depleted patients, in the case of aminoglycosides the onset of injury may be a bit slower, consistent with cumulative dose exposure. In general, ATN is best avoided by limiting the dose of potentially toxic medications (e.g., once-daily dosing of aminoglycosides), maintenance of adequate volume