Nephrol Dial Transplant (2000) 15: 318-323
© 2000 European Renal Association-European Dialysis and Transplant Association
Invited Comments
Tubular cell damage in acute renal failure—apoptosis, necrosis, or both
Department of Medicine, University of Arkansas for Medical Sciences and Central Arkansas Veterans Healthcare System, Little Rock, AR, USA
Correspondence and offprint requests to: Sudhir V. Shah MD, University of Arkansas for Medical Sciences, 4301 W. Markham Street, Slot 501, Little Rock, AR 72205, USA
Keywords: acute renal failure; caspases; cell death; ceramide; endonucleases; reactive oxygen metabolites; renal tubular epithelial cells
Introduction
For almost a century, it has been taken as a foregone conclusion that in ischaemic or toxic injury, renal tubular epithelial (RTE) cells die in a catastrophic breakdown of regulated cellular homeostasis, that is necrosis (Figure 1
). Necrosis is accompanied by massive tissue damage leading to rapid collapse of internal homeostasis of the cell [1]. It is characterized by cell swelling with early loss of plasma membrane integrity, major changes to the organelles, and swelling of the nucleus with flocculation of the chromatin. Affected cells rupture, and the cellular components spill into the surrounding tissue space, evoking an inflammatory response [1,2]. In necrosis, DNA degradation is a later phenomenon, if present, and the chromatin is digested by proteases and endonucleases into a smear pattern instead of a ladder pattern since the proteases destroy the histones and expose the entire length of DNA to
Ischaemic acute renal failure
Other causes of acute renal failure
Role of caspases in RTE cell injury
Role of ceramide in RTE cell injury
Conclusion
Acknowledgments
References
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