There is no evidence to date that the early treatment of streptococcal disease, either pharyngitic or cellulitic, will alter the risk of PSGN. Not all cases of streptococcal infection lead to glomerulonephritis. PSGN usually develops 1-3 weeks following acute infection with specific nephritogenic strains of group A beta-hemolytic streptococcus. The incidence of GN is approximately 5-10% in persons with pharyngitis and 25% in those with skin infection. The characteristic ultrastructural feature of PSGN is subepithelial like dense deposits. By immunofluorescence microscopy, there are granular deposits of IgG, IgM and C3 in the mesangium and along GBM. Focal and sparse immune complex deposits are almost universally present. PSGN does not commonly present with crescent formation. Only in its severe form PSGN may show rapid deterioration of renal function with formation of crescent in the glomeruli It is referred to as rapidly progressive glomerulonephritis.