• Bruce A Molitoris and Timothy A Sutton.
• Division of Nephrology, Department of Medicine, and the Indiana Center for Biological Microscopy, Indiana University School of Medicine, Indianapolis, Indiana 46202, USA. bmolitor@iupui.edu
• Kidney Int. 2004 Aug 1; 66 (2): 496-9.

AbstractThe pathophysiology of ischemic acute renal failure (ARF) involves a complex interplay between renal hemodynamics, tubular and endothelial cell injury, and inflammatory processes. A growing body of evidence supports the contribution of altered renal vascular function, especially at the microvascular level, in initiating and subsequently extending the initial tubular injury. The extension phase of ischemic ARF involves continued reduction in renal perfusion, ongoing hypoxia, and inflammatory processes that occur during reperfusion and contribute to continued tubular cell injury. Vascular endothelial cell injury and dysfunction play a vital part in this extension phase. With injury, the endothelial cell loses its ability to regulate vascular tone, perfusion, permeability and inflammation/adhesion. This loss of regulatory function has a detrimental impact upon renal function. Vascular congestion, edema formation, diminished blood flow, and infiltration of inflammatory cells have been documented in the corticomedullary junction of the kidney. However, linking their genesis to microvascular endothelial injury and dysfunction has been difficult. New diagnostic and therapeutic approaches to ischemic ARF must incorporate these finding to devise early recognition strategies and therapeutic approaches.

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