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 language | English (US) |
---|---|
Pages (from-to) | S56-S61 |
Journal | Kidney International, Supplement |
Volume | 66 |
Issue number | 91 |
DOIs | |
State | Published - Oct 2004 |
Externally published | Yes |
Keywords
- Acute renal failure
- Inflammation
- Ischemia/reperfusion injury
ASJC Scopus subject areas
- Nephrology