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Journal of Transplantation
Volume 2012, Article ID 764154, 7 pages
http://dx.doi.org/10.1155/2012/764154
Review Article

Inflammation and Microvasculopathy in Renal Ischemia Reperfusion Injury

Abteilung für Nephrologie und Rheumatologie, Universitätsklinikum Göttingen, Robert-Koch-Straße 40, 37077 Göttingen, Germany

Received 30 August 2011; Accepted 5 December 2011

Academic Editor: Maciej Kosieradzki

Copyright © 2012 Daniel Patschan et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Acute renal failure (ARF) severely worsens prognosis of hospitalized patients. The most frequent cause of intrarenal ARF is transient or prolonged renal hypoperfusion (ischemia). Ischemia primarily affects the function and structure of tubular epithelial cells, which, in severe cases, is characterized by epithelial cell necrosis. Nevertheless, ischemia does not exclusively lead to alterations of epithelial cells but also causes interstitial inflammation and interstitial microvasculopathy. Both inflammation and microvasculopathy are particularly important in terms of postischemic kidney repair. Postischemic microvasculopathy is characterized by endothelial cell swelling with subsequent microvascular occlusion. Thus, reperfusion is inhibited (no-reflow phenomenon). Such endothelial cell dysfunction offers new therapeutic perspectives in ischemic ARF. Newer observations point towards the role of the so-called endothelial progenitor cells (EPCs) in the treatment of ARF. Systemic administration of EPCs to mice with bilateral renal ischemia mitigates postischemic endothelial cell dysfunction and protects animals from acute renal failure.