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Interferon- Reduces Proteinuria in Experimental Glomerulonephritis

Simon C. Satchell^*, Olena Buchatska, Sarah B. Khan, Gurjeet Bhangal, Candida H. Tasman^*, Moin A. Saleem^*, Darren P. Baker, Roy R. Lobb, Jennifer Smith, H. Terence Cook, Peter W. Mathieson^* and Charles D. Pusey

^* Academic Renal Unit, University of Bristol, Southmead Hospital, Bristol; Renal Section; Department of Histopathology, Imperial College London, Hammersmith Hospital, London, United Kingdom; and Biogen Idec Inc., Cambridge, Massachusetts

Correspondence: Dr. Simon C. Satchell, Academic Renal Unit, University of Bristol, Southmead Hospital, Bristol, BS10 5NB, UK. Phone: +44-117-959-5437; Fax: +44-117-959-5438; s.c.satchell{at}bristol.ac.uk

Received for publication October 10, 2006. Accepted for publication July 11, 2007.

Interferon- (IFN-) is a multifunctional cytokine with immunomodulatory properties. We examined the effect of IFN- in three separate rat models of glomerular injury and in cultured human glomerular endothelial cells and podocytes. In nephrotoxic nephritis in WKY rats, recombinant rat IFN- started either at induction or after establishment of disease significantly reduced 24-h proteinuria by up to 73% and 51%, respectively, but did not affect serum creatinine. There was a slight reduction in numbers of glomerular macrophages, but no difference in glomerular or tubulointerstitial scarring. In Thy-1 nephritis in Lewis rats, IFN- started at induction of disease reduced proteinuria by up to 66% with no effect on numbers of glomerular macrophages, but a reduced number of proliferating cells. In puromycin nephropathy in Wistar rats, IFN- started at induction of disease reduced proteinuria by up to 93%, but had no effect on glomerular histology. In cultured cells, human IFN--1a had a dramatic effect on barrier properties, increasing electrical resistance across monolayers of either glomerular endothelial cells or podocytes and decreasing trans-monolayer passage of albumin. In conclusion, these results show that IFN- reduces proteinuria in three different rat models of glomerular injury and that its anti-proteinuric action may result from direct effects on cells that comprise the glomerular filtration barrier. These data indicate that IFN- may have potential as a therapeutic agent in proteinuric renal disease.

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J. Am. Soc. Nephrol. 2007 18: F3. [Full Text] [PDF]

Copyright © 2008 by the American Society of Nephrology. Online ISSN: 1533-3450 Print ISSN: 1046-6673