Journal
KIDNEY INTERNATIONAL
Volume 66, Issue -, Pages S56-S61Publisher
ELSEVIER SCIENCE INC
DOI: 10.1111/j.1523-1755.2004.09109.x
Keywords
acute renal failure; inflammation; ischemia/reperfusion injury
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Funding
- NIDDK NIH HHS [DK063120] Funding Source: Medline
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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-alpha (TNF-alpha) in mediating the inflammatory injury in cisplatin-induced acute renal failure has recently been established. Cisplatin induces the expression of TNF-alpha and TNF receptor subtype 2 (TNFR2) within the kidney. Genetic deletion of either TNF-alpha 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-alpha might reduce cisplatin-induced renal failure in humans.
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