Three pathogenesis of glomerulonephritis2017-05-06 10:33
Three pathogenesis of glomerulonephritis, experts give the following explanation:
1, immune complex deposition in glomerular epithelial cells:
The epithelial cells were damaged, and the surface of C3b was further induced by a large number of immune complexes deposited to the epithelium, leading to the formation of membranous nephropathy. If only the glomerular epithelial cells were swollen under the light microscope, it was observed that under the electron microscope, the podocyte foot processes were widely fused and flattened.
2, immune complex deposition in the glomerular mesangial area:
A large number of immune complex deposition in the glomerular mesangial area, to attract inflammatory mediators, inflammatory reaction. The damage of mesangial cells and mesangial cell proliferation and contraction. Mesangial cell proliferation, mesangial matrix increased, which is mesangial proliferative glomerulonephritis, at this time if there is proliferation of endothelial cells, that is, capillary proliferative glomerulonephritis. With secretion of medium, matrix increased, capillary lumen stenosis caused by ischemia and hypoxia, and mesangial cells in the medium under the action of inflammatory and stromal differentiation into myofibroblasts, extracellular matrix, disease progression, progression of renal fibrosis; contraction of mesangial cells, resulting in filtration area less filtration fraction reduced basal membrane damage, increased permeability, leakage of useful substances; again the phagocytic function of mesangial cells decreased, which decreased immune function, not large molecules were swallowed, which makes the large accumulation of mesangial cell differentiation into myofibroblasts, secretion is not easy to be degraded ECM, healthy kidney cells the gradual loss of. In conclusion, damaged mesangial cells occupy a central position in renal fibrosis. With the expansion and spread of the injured cells, the healthy renal units of the kidney are less, and the renal fibrosis is progressing gradually.
3, immune complex deposition in glomerular endothelium:
Normal healthy glomerular endothelial cells have their normal functions. When the endothelial cells are damaged, the structure changes and the functions change accordingly. Decreased endothelial cell damage after anticoagulant activity, promote platelet adhesion and aggregation, leading to glomerular capillary micro thrombosis, ischemia and hypoxia; due to impaired NO (nitric oxide), PGI2 (prostacyclin) reduction of vasodilators, secretion of angiotensin increases, causing vasoconstriction, resulting in renal hypertension in addition, the charge barrier; filtration barrier has damaged basement membrane permeability injury. Endothelial cell damage after the three results of interaction, and further lead to local renal microcirculation disorder, some glomerular sclerosis, and hematuria, proteinuria and other clinical manifestations.
Studies have shown that there are many mechanisms of pathogenesis in patients with glomerulonephritis, which is mainly caused by antigen antibody reaction.
Due to various kinds of infections and drugs, antigen antibody binding to form immune complexes, according to their different size and influence charge deposited in different regions of renal intrinsic cells, respectively deposited on the endothelial and mesangial region, subepithelial immune complex deposition position, not broken, the formation damage of kidney cells of different the. According to the nature, location and range of renal lesions, it was divided into different pathological types, minimal change nephropathy, membranous glomerulonephritis and crescentic glomerulonephritis.