ACUTE POSTINFECTIUOS

ACUTE POSTINFECTIUOS (POSTSTREPTOCOCCAL)GNPathogenesis:It is generally that immune complex deposition is involved The relevant antigens are probably streptococcal proteinsPrimary injury result from complement activation, resulting in diffuse proliferation and swelling of glomerular cells and frequent infiltration of leukocytes.Similar proliferative GN are seen in other endogenous and exogenous antigens??Clinical course: the onset is abrupt, proceed by malaise, slight fever, nausea and nephritic syndrome, oliguria, azotemia, and hypertension, gross haematuriaMorphology:Uniformly increased cellularity, of the glommerular tufts result from proliferation and swelling of endothelial and mesangial cells and by neutrophilic and monocytic infiltrate
Pathogenesis:It is associated with an abnormality in IgA production and clearance, is at low lvels in normal individual but increased in 50% of patients with IgA nephropathy, studies suggest an abnormality in glycosylation of the IgA immunoglobulin this will led to reduce plasma clearance of IgA thus fovring deposition in the mesangium, IgA nephropathy occurs with increased frequnciy with celiac diseaseClinical course: often affects childdern and young adults, often with gross haematuria after an infection of the respiratory or??, 30-40% have only micrscopic haematuria, 5-10% develop acute nephritic syndrome , haematuria last for few days and then subside and return every few months Morphology:variable , may show mesangial widening or mesangial proliferation