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Role of endothelin and tumour necrosis factor in the renal response to sepsis.

Abstract
A rapidly increasing body of evidence is implicating endothelin and TNF in the pathogenesis of septic acute renal failure. TNF causes renal damage by recruiting leukocytes, accelerating fibrin accumulation, promoting cell lysis, stimulating the release of vasoconstrictor substances, and other mechanisms. ET-1 causes renal dysfunction in sepsis and endotoxaemia primarily by evoking severe reductions in RBF and GFR. While these are only two of the many agents that mediate renal dysfunction during sepsis, they stand out by virtue of their combined ability to modulate numerous inflammatory pathways and to elicit marked alterations in renal function. Clearly the development of specific TNF and endothelin antagonists holds out promise for the treatment and prevention of septic acute renal failure.
AuthorsD E Kohan
JournalNephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association (Nephrol Dial Transplant) Vol. 9 Suppl 4 Pg. 73-7 ( 1994) ISSN: 0931-0509 [Print] England
PMID7800273 (Publication Type: Journal Article, Review)
Chemical References
  • Endothelins
  • Tumor Necrosis Factor-alpha
Topics
  • Acute Kidney Injury (etiology, physiopathology)
  • Animals
  • Endothelins (physiology)
  • Glomerular Filtration Rate (physiology)
  • Humans
  • Kidney (physiopathology)
  • Leukocytes (physiology)
  • Renal Circulation (physiology)
  • Sepsis (complications, physiopathology)
  • Tumor Necrosis Factor-alpha (physiology)

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