Acute Renal Failure in Cardiovascular and Other Surgical Patients

Abstract

The acute onset of oliguria and azotemia in the postoperative setting may be caused by prerenal or postrenal causes or intrinsic renal damage. The first step in arriving at a diagnosis is to review the history in order to elicit the extrarenal factors. Certain simple laboratory tests are of tremendous value in differentiating these conditions. The development of acute renal failure with renal parenchymal damage usually occurs in the setting of hypotension, sepsis, dehydration, and with exposure to nephrotoxins. Most patients will be excreting scant amounts of isotonic urine containing more than 20 to 30 mEq per liter of sodium. Their urine:plasma creatinine ratio is less than or equal to 20:1 and their urinary sediment reveals many epithelial cells and casts. The condition is usually reversible and the treatment is expectant. However, it is still associated with a high mortality, although the survival of patients with acute renal failure may be substantially higher than previously reported. Early dialysis and nutritional support may play an important role in the improved survival. Patients with nonoliguric acute renal failure have urine outputs that may exceed 2 liters per day. Despite this output they demonstrate a stepwise increase in serum urea and creatinine. Urine sodium and osmolality are not very helpful. Many such patients do have low (less than 20 mEq per liter) urine sodium concentration and excrete isotonic urine.