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

Semin Nephrol. 2004 Jul;24(4):316-23. doi: 10.1016/j.semnephrol.2004.04.003.


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.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Acute Kidney Injury / enzymology*
  • Acute Kidney Injury / etiology
  • Acute Kidney Injury / physiopathology*
  • Biological Availability
  • Endothelium, Vascular / enzymology
  • Endothelium, Vascular / physiopathology
  • Humans
  • Kidney Function Tests
  • Nitric Oxide Synthase / metabolism*
  • Nitric Oxide Synthase Type III
  • Prognosis
  • Risk Assessment
  • Severity of Illness Index


  • NOS3 protein, human
  • Nitric Oxide Synthase
  • Nitric Oxide Synthase Type III