Acute Ischemic Renal Failure: Review of Experimental Studies on Pathophysiology and Potential Protective Interventions

Abstract

More than 70% of acute renal failure in man is of circulatory nature and results from hypoxic injury to the kidney. Since intrarenal hemodynamic and metabolic events cannot be accurately assessed in human acute renal failure, various experimental models of renal hypoperfusion or complete interruption of renal blood supply, such as norepinephrine-induced acute renal failure or clamping of the renal artery, have been employed to obtain more direct insight into the pathophysiological events and consequences of hypoxia, although none of these models may truly mimic human acute renal failure. In addition, the severity of experimental acute renal failure, that is, oliguric or nonoliguric acute renal failure resulting from renal hypoperfusion, depends not only on the model employed but also largely on the experimental conditions. In the hemodynamic models a vascular component is incriminated in the initial phase, and persistent tubular tissue dysfunction in the maintenance phase of ischemic acute renal failure. Hypoxic vascular injury will lead to vasoconstriction; a decrease in glomerular filtration pressure, glomerular capillary surface area, and permeability; and thus to a decrease in glomerular filtration rate. In contrast to previous concepts which incriminated the renal cortex as the main target tissue of hypoxic injury, in recent years attention has been focused on impaired medullary perfusion as the most prominent pathophysiological event leading to the decrease in total renal blood flow and glomerular filtration rate. Medullary congestion may result from hypoxic cell swelling with vascular compression.(ABSTRACT TRUNCATED AT 250 WORDS)