Journal
SEMINARS IN NEPHROLOGY
Volume 27, Issue 3, Pages 286-308Publisher
W B SAUNDERS CO-ELSEVIER INC
DOI: 10.1016/j.semnephrol.2007.02.004
Keywords
TNFR1; TNFR2; ischemia-reperfusion injury; endotoxemia; obstructive nepbropathy; hypertension; diabetic nephropathy; glomerulonephritis; lupus nephritis; ANCA-associated vasculitis
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Funding
- NHLBI NIH HHS [P01HL036028] Funding Source: Medline
- NIDDK NIH HHS [DK051643] Funding Source: Medline
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Tumor necrosis factor (TNF) a is a potent proinflammatory cytokine and important mediator of inflammatory tissue damage. In addition., it has important immune-regulatory functions. Many experimental studies and clinical observations support a role for TNF in the pathogenesis of acute and chronic renal disease. However, given its dual functions in inflammation and immune regulation, TNF may mediate both proinflammatory as well as immunosuppressive effects, particularly in chronic kidney diseases and systemic autoimmunity. Blockade of TNF in human rheumatoid arthritis or Crohn's disease led to the development of autoantibodies, lupus-like syndrome, and glomerulonephritis in some patients. These data raise concern about using TNF-blocking therapies in renal disease because the kidney may be especially vulnerable to the manifestation of autoimmune processes. Interestingly, recent experimental evidence suggests distinct roles for the 2 TNF receptors in mediating local inflammatory injury in the kidney and systemic immune-regulatory functions. In this review the biologic properties of TNF and its receptors, TNF receptors 1 and 2, relevant to kidney disease are summarized followed by a review of the available experimental and clinical data on the pathogenic role of the TNF system in nonimmune and immune renal diseases. Experimental evidence also is reviewed that supports a rationale for specifically blocking TNF receptor 2 versus anti-TNF therapies in some nephropathies, including immune complex-mediated glomerulonephritis.
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