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The pathogenesis of acute nephritis

2017-03-06 14:34

Acute nephritis can be divided into 3 types according to the pathological, its pathogenesis is different.

1 the deposition of anti glomerular basement membrane (GBM) antibody (type I) of more than 30% of patients with GBM RPGN linear immunoglobulin deposition, the main component of IgG, even IgA, often accompanied by C3. It was observed that C3 could be deposited in granular form, and the electron dense deposits were observed under electron microscope. Circulating anti GBM antibody positive.

Animal experiments have shown that the injection of anti GBM antibodies can cause IgG in laboratory animals (GBM) on the line like deposition, and lead to severe pathological processes, rapid RPGN. The antigen of the disease is GBM component, GBM antigen and glomerular basement membrane (TBM) and the lung basement membrane antigen cross, anti GBM antibody can also cause renal interstitial injury and pulmonary hemorrhage (Goodpasture syndrome).

Deposited 2 glomerular immune complexes (type II) the patients about 30% compound immune serum positive for immune examination showed glomerular capillary loop and the kind of immunoglobulin deposition membrane particles, its main composition is IgG, IgM, IgA and C3 occasionally. This type of circulating immune system and (or) in situ immune complexes are associated with the formation of antibodies to antigens (infectious or autoantigens).

3 neutrophils and their cytoplasmic antibody (type III) of the patients with glomerular capillary lack immune deposition, but there are obvious focal segmental necrosis and polymorphonuclear leukocyte infiltration in patients with vasculitis, glomerulonephritis, serum examination of common anti neutrophilic cytoplasmic antibody (ANCA) positive. ANCA can identify the neutrophil membrane surface (proteinase 3), the activation of neutrophils, which can release lysosomal enzymes, elastase and active oxygen free radical GBM degradation; ANCA can lead to increased neutrophil enzyme activity, cell mediated immune response, so the change of ANCA is closely related with disease activity.

To sum up, the disease is a group of syndromes caused by a variety of etiology and pathogenesis. The basic mechanism of the glomerular basement membrane with perforation of crescent formation, infiltration of anti GBM antibodies and immune complex mediated immune response and polymorphonuclear leukocytes and macrophages, causing GBM damage. Protein in blood components (fibrinogen and fibrin etc) macrophages and blood vessels in the kidney to escape a lot, the latter is one of the cell components of crescent, and fibrin deposition plays a key role. The crescent cells began to express the glue gene from 1 to 2 days. At the same time, interstitial fibroblasts by fracture of the kidney into the secretion of collagen fibrosis.

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