Pathogenesis of Oliguric Acute Renal Failure

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Abstract
The intrarenal mechanisms whereby hypotension and a variety of toxins lead to acute, and usually reversible, renal failure have been the subject of many recent investigations. The major mechanisms suggested and examined experimentally are tubular obstruction by interstitial edema or casts of necrotic tubular epithelium, the back flow of largely unaltered glomerular filtrate across denuded or functionally damaged tubular epithelium, and a primary, hemodynamically mediated reduction in glomerular filtration rate. Severe oliguria during acute renal failure usually precludes estimates of renal hemodynamics based on conventional clearance technics. Moreover, measurements of renal blood flow or filtration rate obtained by clearance technics . . .