The role of renal hemodynamic alterations in the curtailment of renal function was studied in rabbits with
uranyl acetate-induced
acute renal failure. The day following the i.v. injection of
uranyl acetate (2 mg/kg of body wt), renal blood flow (RBF) and clearance of
creatinine (Ccr) decreased to approximately 60 and 20% of controls, respectively. Intracortical fractional flow distribution, estimated by radioactive
microsphere method, did not change. The extraction ratio of para-aminohippurate (EPAH) decreased and the renal extraction of
sodium (CNa/Ccr) increased, with minimal structural change in the kidney. Urine output increased to two to three times that of the control. After three days
oliguria appeared despite complete recovery of RBF. The
zonal flow redistributed toward the deep cortex. CCr and EPAH reached their minimums, concomitantly with tubular
necrosis and intratubular casts. After seven days animals could be divided into the oliguric and
diuretic groups. CCr and EPAH were higher in the
diuretic group, while there was no significant difference in RBF and the flow distribution between groups. Regeneration of damagee tubular cells was found in the
diuretic group but not in the oliguric group. The findings suggest the minor roles of RBF and the intracortical flow distribution, and a fundamental role of back leakage of filtrate across damaged tubular epithelium in the maintenance of reduced CCR and urine output during the oliguric stage in rabbits with
uranyl acetate-induced
renal failure.