The role of cell adhesion molecules in ischemic acute renal failure

Abstract

Ischemia remains the primary cause of acute renal failure in adults. Following the development and practical application of dialysis, little progress has been made in the treatment of ischemic acute renal failure (ARF) to significantly affect patient outcome. However, excellent advancement has occurred in the understanding of the cellular consequences of ischemic injury. This has occurred through an integrated approach using complementary in vivo and in vitro models of ischemic cell injury. Fundamental insights into the physiology, biochemistry, cell biology, and molecular biology of ischemic cell injury have now resulted in new clinical trials and renewed optimism. These combined basic science and clinical research approaches to design and test new therapies were recently reviewed to identify priorities by a NIH supported conference ( 1 Dubose Jr, T.D Warnock D.G Mehta R.L et al. Acute renal failure in the 21st century recommendations for management and outcomes assessment. Am J Kidney Dis. 1997; 29: 793-799 Abstract Full Text PDF PubMed Scopus (90) Google Scholar ). Since substantial progress has been made in the pathophysiologic aspects of cell adhesion molecules in the injury and recovery phases of ischemic ARF, the purpose of this review is to delineate and synthesize these findings. Although brief introductions will be given to the different classes of cell adhesion molecules (CAMs), the reader is referred to the original article in this series, which dealt exclusively with the structure and cellular function of these molecules ( 2 Kypta R.M Su H Reichardt L.F Association between a transmembrane protein tyrosine phsophatase and the cadherin-catenin complex. J Cell Biol. 1996; 134: 1519-1529 Crossref PubMed Scopus (234) Google Scholar ).