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The Cellular Basis of Ischemic Acute Renal Failure

  • Alexander Leaf
  • Anthony D. C. Macknight
  • Joseph Y. Cheung
  • Joseph V. Bonventre

Abstract

It has long been recognized that obstruction of the blood supply to the normothermic kidney for periods of greater than 1 hr will almost invariably result in tubular necrosis and the clinical picture of acute renal failure. As the duration of arterial obstruction increases from 30 to 60 min, the proportion of kidneys that suffer damage increases, as does the extensiveness of damage. In the past few years there has been heightened interest in the nature of the lesion(s) caused by ischemia which results in irreversible cell injury even if blood flow to the kidney is restored. Identifying the critical change or changes that doom the cell to certain death will not only add to our knowledge of cellular physiology but possibly provide the basis for therapeutic interventions aimed at preventing or delaying the onset of the irreversible change(s). It is this latter hope that has done much to stimulate research.

Keywords

Acute Renal Failure Ischemic Injury Adenine Nucleotide Ischemic Insult Ehrlich Ascites Tumor Cell 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Plenum Publishing Corporation 1986

Authors and Affiliations

  • Alexander Leaf
    • 1
  • Anthony D. C. Macknight
    • 2
  • Joseph Y. Cheung
    • 1
  • Joseph V. Bonventre
    • 1
  1. 1.Department of MedicineHarvard Medical School and Massachusetts General HospitalBostonUSA
  2. 2.Department of PhysiologyUniversity of Otago Medical SchoolDunedinNew Zealand

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