Seminars in Nephrology
Volume 24, Issue 4 , Pages 316-323, July 2004

NO bioavailability, endothelial dysfunction, and acute renal failure: new insights into pathophysiology

  • Michael S Goligorsky

      Affiliations

    • Department of Medicine, New York Medical College, Valhalla, NY, USA
    • Department of Pharmacology, New York Medical College, Valhalla, NY, USA
    • Corresponding Author InformationAddress reprint requests to Michael S. Goligorsky, MD, PhD, Division of Nephrology and Renal Research Institute, New York Medical College, Basic Sciences Building, Valhalla, NY 10595 USA
  • ,
  • Sergey V Brodsky

      Affiliations

    • Department of Medicine, New York Medical College, Valhalla, NY, USA
  • ,
  • Eisei Noiri

      Affiliations

    • Department of Medicine, The University of Tokyo, Tokyo, Japan

Abstract 

This brief overview sketches current evidence of imbalance between inducible nitric oxide synthase (iNOS) and endothelial nitric oxide synthase (eNOS), role of oxidant stress, and generation of peroxynitrite in the pathophysiology of acute ischemic renal injury. The development of endothelial cell dysfunction at early stages of experimental acute renal ischemia is the focus of the review, with the results of recent studies on amelioration of renal injury by the infused endothelial cells engrafting in the renal microcirculation. Finally, this article provides some future perspectives on the potential usefulness of endothelial progenitor cells in the prevention and treatment of acute renal failure.

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 Supported in part by National Institutes of Health grants DK52783, DK45462, and DK45659 (M.S.G.), and an American Heart Association Fellowship 0120200T (S.V.B.).

PII: S0270-9295(04)00051-8

doi:10.1016/j.semnephrol.2004.04.003

Seminars in Nephrology
Volume 24, Issue 4 , Pages 316-323, July 2004