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The majority of primary glomerulonephritides is mediated by the deposition of circulating or in situ formed immune complexes, which may be confirmed by immunofluorescence finding of glomerular granular immune deposits. Their composition and electron microscopically defined localization identify various forms of immune complex glomerulonephritides with different courses and prognoses. Acute postinfectious glomerulonephritis is endocapillary proliferative glomerulonephritis characterized by subepithelial hump-like deposits. The most frequent form of primary glomerulonephritis is IgA glomerulonephritis, which tends to be focal or irregular diffuse mesangial proliferative glomerulonephritis with dominant IgA deposits in the mesangium. Mesangiocapillary proliferative (membranoproliferative) glomerulonephritis is characterized by double contours of the glomerular basement membrane and subendothelial immune deposits. Mesangiocapillary proliferative (membranoproliferative) glomerulonephritis with intramembranous dense deposits and still unclear etiopathogenesis has a similarly unfavourable prognosis. Crescentic extracapillary proliferative glomerulonephritis is the most severe form of glomerulonephritis with a rapidly progressive clinical course. Its development is a consequence of glomerular capillary necrosis and fibrin exudation. It may represent an unfavourable variant of immune complex proliferative glomerulonephritides. In 1−2% it is mediated by anti-glomerular basement membrane antibodies and is characterized by linear glomerular immune deposits. In 5−7% of cases, extracapillary crescentic glomerulonephritis is pauci-immune and is associated with antineutrophil cytoplasmic antibodies. Membranous glomerulonephritis is the only immune complex glomerulonephritis which does not involve a proliferative inflammatory reaction. It is characterized by subepithelial immune deposits and diagnostic changes in the glomerular basement membrane. Its clinical presentation is nephrotic syndrome, similarly to two other nonproliferative forms of glomerulonephritis with unclear etiopathogenesis: minimal change glomerulopathy with favourable prognosis in most cases and focal segmental glomerulosclerosis, mostly with unfavourable prognosis due to poor response to corticosteroids. Kidney biopsy enables the most precise and reliable diagnosis of glomerulonephritis and determination of its pathogenesis, and also provides quantitative assessment of irreversible sclerotic lesions and active, potentially reversible inflammatory changes. It also provides important data for clinical decision regarding the most appropriate therapy and the prognosis.