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 [1,2]. Recent elegant work by Professor Cook and others from Imperial College London has identified genetic factors controlling innate immune responses [3,4] and intrinsic renal cell biology  that contribute to the exquisite susceptibility of Wistar Kyoto (WKY) rats to development of crescentic glomerulonephritis.
|Pages (from-to)||3065 - 3066|
|Number of pages||2|
|Journal||Nephrology Dialysis Transplantation|
|Publication status||Published - 2008|