Mechanisms for oliguria in acute renal failure.

Warm ischemic (90 minutes) acute renal failure (ARF) was evaluated in the dog and found to cause polyuric ARF in the injured kidney if the opposite normal kidney was removed. In contrast, if the normal kidney were left intact, oliguric ARF was noted in the injured kidney. To further evaluate the mechanisms for oliguria and polyuria, chronic reinfusion of urine from a normal kidney into the inferior vena cava (ureterocaval anastomosis) resulted in polyuria in the opposite warm ischemic injured kidney; whereas chronic reinfusion of urine into the portal vein (ureteroportal anastomosis) resulted in profound oliguria in the opposite injured kidney. In separate additional experiments, urine acutely infused into the inferior vena cava at a rate of 0.38 ml/minute caused a significantly greater diuretic and renal hemodynamic response than seen with urine infused into the portal vein. Acute infusions of urea solution (0.38 ml/minute) with the same osmolality of urine were completely devoid of diuretic and renal hemodynamic effects. These studies reveal that urine contains a powerful hemodynamic and diuretic factor which appears to convert oliguric to polyuric ARF following warm ischemic renal injury in the dog. This factor is not urea and can be destroyed by the liver.