genitourinary disorders
Acute Tubular Necrosis (ATN)
Diagnosis of Acute Tubular Necrosis
Differentiation from prerenal azotemia, based mainly on laboratory findings and, in the case of blood or fluid loss, response to volume expansion Acute tubular necrosis is suspected when serum creatinine rises≥0.3 mg/dL/day (26.5 micromol/liter [μmol/L]) above baseline or a 1.5- to 2.0-fold increase in serum creatinine from baseline after an apparent trigger (eg, hypotensive event, exposure to a nephrotoxin); the rise in creatinine may occur 1 to 2 days after certain exposures (eg, IV radiocontrast) but be more delayed after exposure to other nephrotoxins (eg, aminoglycosides). ATN must be differentiated from prerenal azotemia because treatment differs. In prerenal azotemia, renal perfusion is decreased enough to elevate serum bloodureanitrogen (BUN) out of proportion to creatinine, but not enough to cause ischemic damage to tubular cells. Prerenal azotemia can be caused by direct intravascular fluid loss (eg, due to hemorrhage, gastrointestinal tract losses, urinary losses) or by a relative decrease in effective circulating volumewithoutloss of total body fluid (eg, in heart failure, portal hypertension with ascites). If fluid loss is the cause, volume expansion using IV normal saline solution increases urine output and normalizes serum creatinine level. If ATN is the cause, IV saline typically causes no increase in urine output and no rapid change in serum creatinine. Untreated prerenal azotemia may progress to ischemic ATN. Laboratory findings also help distinguish acute tubular necrosis from prerenal azotemia (see table). 