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* Section of Nephrology, Department of Medicine, and
Section of Transplantation Surgery, University of Chicago, Chicago, IL 60637
Bacterial endotoxin (LPS) is responsible for much of the widespread inflammatory response seen in sepsis, a condition often accompanied by acute renal failure (ARF). In this work we report that mice deficient in TNFR1 (TNFR1-/-) were resistant to LPS-induced renal failure. Compared with TNFR1+/+ controls, TNFR1-/- mice had less apoptosis in renal cells and fewer neutrophils infiltrating the kidney following LPS administration, supporting these as mediators of ARF. TNFR1+/+ kidneys transplanted into TNFR1-/- mice sustained severe ARF after LPS injection, which was not the case with TNFR1-/- kidneys transplanted into TNFR1+/+ mice. Therefore, TNF is a key mediator of LPS-induced ARF, acting through its receptor TNFR1 in the kidney.
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