Free-radical-mediated postischemic reperfusion injury in the kidney

Roman E. Ratych, Gregory B. Bulkley

Research output: Contribution to journalArticle

Abstract

Acute tubular necrosis is a frequent occurrence following hypovolemic shock and human renal transplantation. Although this postischemic injury was originally thought to result from ischemia alone, it has recently been recognized that significant tissue injury can occur during the period of reperfusion. The demonstration of the oxygen free-radical-mediated postischemic reperfusion injury by Granger, Rutili, and McCord in ischemic cat intestine suggested that this mechanism might also be operative following renal ischemia. In the kidney, postischemic injury results in necrosis of the proximal renal tubule and accumulation of erythrocytes in the outer renal medulla. It has been proposed that the primary event leading to these pathologic changes is a free-radical-mediated injury to the endothelial cells in the inner stripe of the outer medulla. Experimental evidence in animals subjected to warm and cold ischemia supports a free-radical-mediated mechanism. The clinical significance of these findings is demonstrated in preclinical animal studies of renal transplantation in which approximately two-thirds of the injury following cold ischemia could be ablated by superoxide dismutase administered just prior to reperfusion or by allopurinol when administered both at the time of preservation and reperfusion or at the time of preservation alone.

Original languageEnglish (US)
Pages (from-to)311-319
Number of pages9
JournalJournal of Free Radicals in Biology and Medicine
Volume2
Issue number5-6
DOIs
StatePublished - 1986

Keywords

  • Allopurinol
  • Cold renal ischemia
  • Ischemia
  • Kidney
  • Oxygen free radicals
  • Superoxide dismutase
  • Tissue injury
  • Warm renal ischemia
  • reperfusion

ASJC Scopus subject areas

  • Biochemistry

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