The study of oliguric and polyuric acute renal failure

A simple laboratory model for acute renal failure (ARF) induced by warm ischemia was studied in an attempt to elucidate the mechanisms for oliguria. It was observed that unilateral warm ischemic injury with contralateral nephrectomy or bilateral warm ischemic injury resulted in a high output (polyuric) form of ARF. In contrast, when unilateral warm ischemic injury was induced and the contracolateral kidney was left intact, low output (oliguric) ARF was observed in the injured kidney. Ligation of the ureter of the normal contralateral kidney reversed the oliguric state. Replacement of the urine output by the normal kidney with Ringer's lactate solution failed to reverse the low output state in the injured kidney. Reinfusion of the urine itself from the intact contralateral kidney, while increasing urine output, did not entirely alleviate the oliguric phenomenon in the injured kidney during a 24-hr period during which the animals underwent volume expansion. Although the basis for the oliguria in the injured kidney when functioning renal tissue remains is unclear, indirect evidence suggests that the excretion of a diuretic factor in urine by the normal kidney contributes to the oliguria observed in the injured kidney.