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The term crescentic glomerulonephritis (CrGN) refers to a diverse collection of disorders of widely different etiology and pathogenesis having in common the development of extensive proliferation of cells within Bowman's space (Couser, 1988; Glassock et al., 1995; Nachman et al., 1998; Pusey and Rees, 1998; Morgan et al., 2006; Lionaki, et al., 2007). The resulting accumulation of cells gives rise to a ‘crescent’ enveloping the glomerular tuft itself. Polymerization of fibrinogen in Bowman's space due to passage of fibrinogen through gaps in the capillary wall, the elaboration of procoagulant factors by infiltrating monocytes and impaired fibrinolysis all contribute to the pathogenesis of the crescent (Couser, 1988, Glassock et al., 1995). Usually 〉50% of glomeruli are involved with crescentic lesions. Such patients also frequently manifest rapid and progressive deterioration of renal function leading to the clinical syndrome of rapidly progressive glomerulonephritis. Early and aggressive treatment can often delay or prevent the development of end-stage renal disease (ESRD). See Table 10.1 for an etiologic and pathogenetic classification of CrGN. |
