Inflammatory cytokines in acute renal failure

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.