NDT Advance Access originally published online on July 25, 2008
Nephrology Dialysis Transplantation 2008 23(10):3065-3066; doi:10.1093/ndt/gfn402
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© The Author [2008]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org
Crescentic nephritis—is it in your genes?*
Centre for Inflammatory Diseases, Monash University, Clayton, Victoria, Australia
Peter Tipping, Centre for Inflammatory Diseases, Monash University, Clayton, Victoria, Australia. Tel: +61395945547; Fax: +61395946495; E-mail: peter.tipping@med.monash.edu.au
Keywords: genetics; JunD; macrophage; Wistar–Kyoto; glomerulonephritis
| The first 10% of the full text of this article appears below. |
Crescentic glomerulonephritis is frequently associated with a rapid clinical course and poor outcome, particularly if treatment is delayed. The severity of the renal injury and the suboptimal treatment modalities for this disease have provided considerable impetus to studies of the underlying immuno-pathogenic mechanisms. Well-documented variation in susceptibility to crescentic glomerulonephritis between inbred strains of rodents has strongly suggested the influence of genetic predisposing factors in animal models. In mice, susceptibility to crescentic disease in strains showing strong Th1 responses to nephritogenic antigens indicates that genetic factors may operate (in part) through regulation of adaptive T helper subset responses