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The diminished glomerular filtration rate observed in previous studies of acute renal failure induced by uranyl nitrate has been ascribed to backflow of glomerular filtrate through necrotic tubular epithelium, since renal blood flow was essentially normal. Renal blood flow (133xenon washout) and renal function were studied serially for 96 hours after the administration of uranyl nitrate (10 mg/kg, iv) in unanesthetized dogs with chronic renal artery catheters. Inulin clearance and total renal blood flow decreased to 25% and 52% of control, respectively, by 6 hours and remained depressed. By 3 hours, cortical flow decreased to 330±20 ml/min 100 g-1 (control 507±12 ml/min 100 g−1) and outer medullary flow increased to 147±8 ml/min 100 g−1 (control 97±18 ml/min 100 g-1), indicating intrarenal blood flow redistribution. From 6 hours on, these flow components were no longer separable. The ratio of flow in the outer two-thirds of the renal cortex to that in the whole cortex, determined using 85strontium-labeled microspheres (15μ), decreased to 0.34±0.06 and 0.40±0.04 at 6 and 96 hours, respectively (control 2.21±0.12). Plasma renin activity was 1.8±0.6 ng/ml hour−1 at 3 hours and remained elevated (control 0.6±0.2 ng/ml hour−1). Histological examination revealed minimal tubular change at 6 hours and widespread disruption at 96 hours. The decrease in renal blood flow prior to any significant tubular pathology suggests that alterations in renal hemodynamics, which may be mediated by the renin-angiotensin system, are responsible for the diminished renal function observed in this model of acute renal failure.

Experimental Acute Renal Failure Induced by Uranyl Nitrate in the Dog