Inflammatory cytokines in acute renal failure

Ganesan Ramesh, W. Brian Reeves

Research output: Contribution to journalReview articlepeer-review

170 Scopus citations


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)
Pages (from-to)S56-S61
JournalKidney International, Supplement
Issue number91
StatePublished - Oct 2004
Externally publishedYes


  • Acute renal failure
  • Inflammation
  • Ischemia/reperfusion injury

ASJC Scopus subject areas

  • Nephrology


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