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【Objective】To establish the model of rats of Hepatitis B Virus-Associated Glomerulonephritis, and to research the method of establishing animal model of Hepatitis B Virus-Associated Glomerulonephritis, and to analyze the pathological mechanism.【Methods】20 male SD rats, weight 200g, received food and water. After one week, then they were divided into two groups randomly: the normal group, model group. Model rats were induced by injection of HBsAg, HBeAg positive serum via tail veins, 0.75ml/100g, twice a week for 4 weeks. The rats of health control group were given injection of physiological saline, in the same way. Observation indices included main symptoms and signs, urinary protein. Before and after building models, they are measured weekly. When the model rats had proteinuria, they were diagnosed nephrotitis, and after one week, we dissected two groups, and took their kidney tissue, and observed them at Light Microscopic, Immunoflu-orescent microscopy, immunohistochemical, and electron microscopic.【Resorts】Compared with that of normal control group, the model groups showed proteinuria, and the pathology inspection observed at Light Microscopic the proliferation of mesangial cell, infiltration of inflammatory cells, protein cast et, and at PASM-Masson deposition of circulating immune complexes in the mesangial area, glomerular basement membrane, subepithelial and endothelial, and the heterogeneity thickness of glomerular basement membrane, and the immunofluorescence showed deposition of IgM (+~++), and IgG (++~+++) in the mesangial area and glomerular basement membrane. Immunohistochemical showed HBsAg deposition a lot tan matter in GBM, mainly in peripheral capillaries. Electron microscopic showed the heterogeneity thickness of glomerular basement membrane, and deposition of immune complexes with lump in the mesangial area, glomerular basement membrane, subepithelial and endothelial. Proteinuria was negative in all control rats. And the control group was negative in Light microscopic, immunofluorescence, immunohistochemical, and electron microscopic.【Conclusion】The hepatitis B virus-associated glomerulonephritis rats model can be established by injection of HBsAg, HBeAg positive serum via tail veins, by imitating replication process of HBV in the body. The deposition of HBV antigen/antibody complex in kidney is one of the pathological mechanisms of hepatitis B virus-associated glomerulonephritis, and atypical membranous nephropathy is the major pathologic type.
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