ATN is a nonspecific renal tubular lesion in response to a variety of renal insults. ATN is caused by a variety of etiologies the most common being ischemic renal hypoperfusion (hypovolemia or decreased cardiac output), aminoglycoside induced nephrotoxicity, iodinated radiocontrast dye induced nephrotoxicity and rhabdomyolysis (myoglobin induced nephrotoxicity). ATN is divided into three distinct stages: (1) renal failure phase, (2) diuretic phase, and (3) recovery phase.

The renal failure phase is characterized by the rapid onset of acute renal failure and all of the associated symptoms and complications. The patient then progresses to the second phase, the diuretic phase. This usually occurs after 7 to 21 days but may be delayed for up to 3 to 6 months. The diuretic phase is characterized by an improvement in renal function, as evidenced by a reduction in the serum BUN and creatinine, and a progressive increase in urine output. If urine output increases and the creatinine remains elevated or continues to rise, this may be indicative of a decrease in tubular resorption and does not represent progression to the diuretic phase. It is imperative to monitor and maintain hemodynamics during the diuretic phase as patients may generate excessive urine volumes, which if not replaced, may lead to dehydration and a secondary rise in BUN and Cr from renal hypoperfusion.

ATN, regardless of the etiology, may be classified as oliguric or nonoliguric. The difference is the urine volume. Patients with oliguric ATN have a daily urine output less than 500 cc per day. The presence of spontaneous nonoliguric ATN is indicative of less severe renal damage and a better prognosis. However, the conversion of oliguric ATN to nonoliguric ATN via the use of diuretics does not improve the prognosis.