Pathogenesis of glomerulonephritis

1, immune complex deposition in glomerular epithelial cells:Epithelial cells are damaged, the surface of the C3b receptor will further induce a large number of immune complex deposition to the epithelium, leading to the formation of membranous nephropathy. If only under the optical microscope glomerular epithelial cell swelling, electron microscopy can be seen under the extensive integration of epithelial cell fossa flattened, compared with minimal changes in kidney disease, the vast majority of cases the prognosis is good.

2, immune complex deposition in the glomerular mesangial area:A large number of immune complex deposition of glomerular mesangial area, to attract inflammatory mediators infiltration, resulting in inflammatory response. Leading to renal mesangial cell damage, so that mesangial cell proliferation, contraction. Mesangial cell proliferation, mesangial matrix increased, which is mesangial proliferative glomerulonephritis, this time if there is endothelial cell proliferation, is the capillary hyperplastic glomerulonephritis.  

With the cell secretion of the media, increased matrix, capillary stenosis, resulting in ischemia and hypoxia, while mesangial cells in the inflammatory mediator and matrix under the role of phenotype into myofibroblasts, a large number of extracellular matrix production, Conditional deterioration, renal fibrosis progress; mesangial cell contraction, resulting in less filtration area, filtration scores decreased, the basement membrane damage, increased permeability, useful material leakage; and then the phagocytic function of mesangial cells decreased, So that the immune function decreased, macromolecules can not be swallowed, a large number of accumulation eventually make the mesangial cell phenotype into myofibroblasts, the secretion of ECM is not easy to be degraded, healthy kidney function of the gradual loss of cells. 

In conclusion, damaged mesangial cells occupy a central position in renal fibrosis. With the expansion of the damaged cells and spread, the kidney of the healthy nephrons less, kidney fibrosis gradually progress.

3, immune complex deposition in the glomerular subcutaneous:Normal healthy glomerular endothelial cells have their normal function, when the endothelial cells are damaged, the structure changes, the function also changes accordingly. After the damage of endothelial cells decreased anticoagulant activity, promote platelet adhesion and aggregation, leading to glomerular capillary microthrombosis, ischemia and hypoxia; Moreover, due to damage, NO (nitric oxide), PGI2 (Prostacyclin) and other vasodilator factors to reduce the secretion of angiotensin increased, leading to vasoconstriction, resulting in renal hypertension; In addition, the damaged charge filtration barrier obstruction, basement membrane injury increased permeability. 

Endothelial cells damaged after the three results of interaction, and further lead to local renal microcirculation, partial glomerular sclerosis, and the emergence of hematuria, proteinuria and other clinical manifestations.Studies have shown that the pathogenesis of glomerulonephritis in many ways, mainly for the antigen-antibody response caused by allergic reactions.

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