Crescentic glomerulonephritis is not a specific disease but rather is a morphologic expression of severe glomerular injury that can be caused by many different aetiologies and pathogenic mechanisms w1, 2x. The major pathogenic event that causes crescent formation is rupture of glomerular capillaries, which allows cellular and humoral inflammatory mediators to spill into Bowman’s space. Because this structural phenotype indicates severe glomerular injury, it is not surprising that it usually correlates with clinical manifestations of severe active glomerulonephritis and rapid loss of renal function, ie rapidly progressive glomerulonephritis. Rapid and accurate diagnosis of crescentic glomerulonephritis, which must include precise subclassification, is essential for optimum renal and patient outcome. This is reflected in the strong correlation between outcome and the serum creatinine at the time of initiation of treatment. On the basis of immunopathologic findings, crescentic glomerulonephritis can be classified into three major categories: immune complex glomerulonephritis, anti-glomerular basement membrane antibody (anti-GBM) glomerulonephritis, and pauciimmune glomerulonephritis, which often is associated with antineutrophil cytoplasmic autoantibodies (ANCA) w1, 2x. Each of these categories can be further divided based on clinical, pathologic and serologic findings (Figure 1). This categorization is useful for clinical management of crescentic glomerulonephritis.