Journal
EUROPEAN JOURNAL OF CLINICAL INVESTIGATION
Volume 38, Issue -, Pages 39-44Publisher
WILEY
DOI: 10.1111/j.1365-2362.2008.02007.x
Keywords
Acute kidney injury; acute renal failure; endotoxin; TLR4; toll-like receptors
Funding
- National Institute of Diabetes and Digestive and Kidney Diseases [IRO1 DK60495-01A1, P30 DK079312-01]
- DCI research fund
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK060495, P30DK079312] Funding Source: NIH RePORTER
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Acute renal failure is a grave complication of systemic gram-negative sepsis. The pathophysiological mechanisms of sepsis leading to kidney injury result in part from systemic inflammatory and haemodynamic alterations. These are triggered by the interaction of endotoxin with Toll-like receptor 4 (TLR4) on cells of the immune system. Recently, TLR4 and other co-effector molecules were identified on renal tubular and vascular cells. Furthermore, it was demonstrated that systemic endotoxin has direct access to renal sites where these receptors are expressed. Therefore, we review data in support of this novel pathway of renal injury in sepsis, whereby systemic endotoxin causes direct injury through interactions with local epithelial and endothelial TLR4.
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