Inflammatory cytokines in acute renal failure

Ganesan Ramesh, W. Brian Reeves

Research output: Contribution to journalReview article

120 Citations (Scopus)

Abstract

A growing body of evidence indicates that inflammatory mechanisms contribute to toxin-induced acute renal failure as well as ischemia/reperfusion injury. A role for tumor necrosis factor-α (TNF-α) in mediating the inflammatory injury in cisplatin-induced acute renal failure has recently been established. Cisplatin induces the expression of TNF-α and TNF receptor subtype 2 (TNFR2) within the kidney. Genetic deletion of either TNF-α or TNFR2 substantially reduces cisplatin-induced renal failure and also necrosis and apoptosis within the kidney. Studies will be required to determine if pharmacologic inhibition of TNF-α might reduce cisplatin-induced renal failure in humans.

Original languageEnglish (US)
JournalKidney International, Supplement
Volume66
Issue number91
StatePublished - Oct 1 2004

Fingerprint

Tumor Necrosis Factor Receptors
Acute Kidney Injury
Cisplatin
Cytokines
Renal Insufficiency
Tumor Necrosis Factor-alpha
Kidney
Reperfusion Injury
Necrosis
Apoptosis
Wounds and Injuries

Keywords

  • Acute renal failure
  • Inflammation
  • Ischemia/reperfusion injury

ASJC Scopus subject areas

  • Nephrology

Cite this

Inflammatory cytokines in acute renal failure. / Ramesh, Ganesan; Reeves, W. Brian.

In: Kidney International, Supplement, Vol. 66, No. 91, 01.10.2004.

Research output: Contribution to journalReview article

Ramesh, Ganesan ; Reeves, W. Brian. / Inflammatory cytokines in acute renal failure. In: Kidney International, Supplement. 2004 ; Vol. 66, No. 91.
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