第一章 丁小强-肾小球疾病.ppt

肾小球疾病 Glomerular Diseases 丁小强 复旦大学附属中山医院 Why does CIC deposit in the glomeruli? Large area of glomerrular capillaries --more chances to contact Net structure of CIC --easy to deposit and settle down Clearance dysfunction of mesangial cells, disability of mononuclear macrophage, component or function defect of complements Decrease clearance of CIC Balance between the deposit and clearance of IC determines the situation of the diseases Persistence of antigen Clearance dysfunction of mesangial cells disability of mononuclear macrophage component or function defect of complements IC deposit clearance Inflammation Mediators of inflammation A group of molecules which act as mediators of inflammation and complicated biological function Origin of inflammation mediators in kidney Extrinsic Cells in kidney infiltrative neutrophil, lymphocyte, mononuclear macrophage , platelet Intrinsic cells in kidney Mesangial cells, tubular cells, endothelial cells  Mediators of inflammation   - active oxygen and active nitrogen - lipids - complements - cytokines - chemotatic factors  - adhesion molecules  - growth factors - vasoactive substances To arouse or promote - proliferation of cells - accumulation of extracellular matrix - changes of histological structure - expression of immunomodulating molecules and adhension molecules Mechanisms of Primary GN Pathological changes LM Mesangial cells, matrix of mesangium Epithelial cells Endothelial cells Basement membrane Loops of glomeruli EM Foot process Basement membrane Hyperplasy of mesangium (electron-dense deposits ) IF Sites, appearances and types of the deposit (Ig or C) Pathological types of primary GN Minimal change glomerulonephritis Focal segmenta