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NDT Advance Access originally published online on July 2, 2009
Nephrology Dialysis Transplantation 2009 24(9):2634-2636; doi:10.1093/ndt/gfp326
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© The Author [2009]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org


RAS meets SLE*

Rudolf P. Wüthrich

Division of Nephrology, University Hospital, Zürich, Switzerland

Correspondence and offprint requests to: Rudolf P. Wüthrich; E-mail: rudolf.wuethrich@usz.ch

Keywords: renin-angiotensin system (RAS); lupus; inflammation

The first 10% of the full text of this article appears below.



   Role of the type 1 angiotensin receptor AT1 in immune-mediated glomerular injury
 
The renin-angiotensin system (RAS) plays an important role in the pathogenesis of glomerular diseases. To delineate more precisely the role of RAS in creating renal injury, knockout mouse strains lacking the angiotensin type 1 or type 2 receptors (AT1 and AT2) have proven very informative.

Hence, in their elegant study that was published in the April 2009 issue of the Journal of Clinical Investigation, Crowley et al. have tested the effect of a targeted disruption of the AT1 receptor on the glomerular disease process in a mouse lupus nephritis model [1]. MRL-Faslpr/lpr mice develop a severe lupus-like autoimmune syndrome that is characterized by severe proliferative immune-complex glomerulonephritis, autoantibody production and arthritis, in addition to a peculiar lymphoproliferative phenotype.

In their study, a . . . [Full Text of this Article]



   SLE, hypertension and the RAS
 


   Role of RAS inhibition in immune/inflammatory renal injury
 

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