3068 3069 Postinfectious GN is caused by deposition or formation of im- 3070 mune complexes containing microbial antigens, which induce 3071 infiltration of leukocytes and proliferation of glomerular cells. 3072 The most common underlying infections are streptococcal, but the 3073 disorder may also be associated with other infections. Poststrepto- 3074 coccal GN is decreasing in frequency in the United States due to 3075 early antibiotic treatment but continues to be a fairly common dis- 3076 order worldwide. It usually appears 1 to 4 weeks after a streptococcal 3077 infection of the pharynx or skin (impetigo). Skin infections are 3078 commonly associated with overcrowding and poor hygiene. Post- 3079 streptococcal glomerulonephritis occurs most frequently in chil- 3080 dren 6 to 10 years of age, but children and adults of any age can be 3081 affected. 3082 3083 3084 ## Pathogenesis 3085 3086 Poststreptococcal GN is caused by immune complexes containing streptococcal antigens and specific antibodies. Only certain strains of group A β-hemolytic streptococci are nephritogenic, more than 90% of cases being traced to types 1, 4, and 12, which can be identified by typing of the M protein of the bacterial cell walls. 3087 3088 Many lines of evidence support an immunologic basis for post-streptococcal glomerulonephritis. The latent period between infection and onset of nephritis is compatible with the time required for the production of antibodies and the formation of immune complexes. Elevated titers of antibodies against one or more streptococcal antigens are present in a great majority of patients. Serum complement levels are low, compatible with activation of the complement system and consumption of complement components. There are granular immune deposits in the glomeruli, indicative of an immune complex-mediated mechanism. 3089 3090 The preponderance of evidence suggests streptococcal pyogenic exotoxin B (SpeB) is the principal antigen in most but not all cases of poststreptococcal glomerulonephritis. This protein is commonly secreted by nephritogenic strains of streptococci, and has been lo-calized to the "humplike" deposits characteristic of this disease (described later). At the outset, the inciting antigens are exoge-nously planted from the circulation in subendothelial locations in glomerular capillary walls, leading to in situ formation of immune complexes, where they elicit an inflammatory response. Subse-quently, through mechanisms that are not well understood, the antigen-antibody complexes dissociate, migrate across the GBM, and reform on the subepithelial side of the GBM. Deposition of 3091 3092 3093 3094 3095 ## TABLE 20.5 Summary of Major Primary Glomerulonephritides 3096 3097 3098

	Most Frequent Clinical Presentation	Pathogenesis	Glomerular Pathology
Disease			Light Microscopy	Fluorescence Microscopy	Electron Microscopy
Postinfectious glomerulonephritis	Nephritic syndrome	Immune complex-mediated; circulating or planted antigen	Diffuse endocapillary infiltration	Granular IgG and C3 in GBM and mesangium; Granular IgA in some cases	Primarily subepithelial rami; subendothelial deposits in early house-stage
Crescentic (rapidly progressive) glomerulonephritis	Nephritic syndrome; rapid progression	Anti-GBM antibody-mediated; immune [... Output truncated due to length. 4589 tokens/17472 characters removed ...]