Oliguria in Patients with Normal Renal Function

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Abstract
Oliguria is common in critically ill patients and may result from prerenal, renal, and postrenal causes. Oliguria also frequently develops in patients with normal concentrations of blood urea nitrogen and creatinine. Most of these patients do not develop renal failure. The authors prospectively studied 100 patients admitted to the ICU to determine the etiology of oliguria in these patients. Eighteen patients (18%) developed oliguria (< 0.33 ml .cntdot. kg-1 .cntdot. h-1 .times. 2 h). Seven and eleven patients were felt on clinical assessment to be hypovolemic or normovolemic, respectively. Compared with the hypovolemic patients, the normovolemic oliguric patients had significantly lower serum osmolalities (278 .+-. 3 vs. 290 .+-. 5 mOsm/kg H2O) and serum sodium concentrations (138 .+-. 3 vs. 132 .+-. 1 mEq/l). In addition, normovolemic patients had significantly higher urine sodium concentrations (83 .+-. 12 vs. 13 .+-. 2 mEq/l), fractional excretion of sodium (1.14 .+-. 0.2 vs. 0.15 .+-. 0.03), and renal failure indices (1.5 .+-. 0.3 vs. 0.21 .+-. 0.04). ADH concentrations in six hypovolemic and six normovolemic patients were increased in both groups but not significantly different. The hypovolemic patients increased their urine output from 17 .+-. 2 ml/h to greater than 0.5 ml .cntdot. kg-1 .cntdot. h-1 following a 500-ml bolus of normal saline. The normovolemic oliguric patients remained oliguric following the saline bolus (13 .+-. 2 to 19 .+-. 3 ml/h). The authors conclude that oliguria is common in critically ill patients and results from renal hypoperfusion and ADH excess. Urine sodium, fractional excretion of sodium, and renal failure index are not useful for predicting renal failure in these patients but are useful for separating the two prerenal etiologies for oliguria.