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肾小球肾炎(即肾炎)发病机理的探讨;对推动肾炎的临床研究有极其重要的地位。近20多年来随着超微结构病理学和免疫化学的进展,特别是动物实验性肾炎模型的复制成功,由于实验动物肾炎与人类肾炎的临床和病理极为相似,使人们更充分地认识到肾炎的发病机理是一种自身免疫反应性疾病。人类肾炎根据其免疫发病机理,过去认为主要有免疫复合物肾炎和抗基底膜肾炎两大类型。免疫复合物肾炎是由于循环中抗原和相应的抗体结合形成免疫复合物,沉积于肾小球基底膜上,激活补体造成肾小球基底膜损伤,由于通透性增高,免疫复合物沉积到肾小球基底膜外侧的上皮足突下所
Glomerulonephritis (ie, nephritis) pathogenesis; to promote the clinical research of nephritis has an extremely important position. In recent 20 years, with the progress of ultrastructural pathology and immunochemistry, in particular the successful replication of experimental animal model of nephritis, the clinical and pathological features of experimental animal nephritis and human nephritis are very similar, which make people more fully recognize nephritis The pathogenesis is an autoimmune disease. According to its pathogenesis of human immunodeficiency, human nephritis in the past that there are two major types of immune complex nephritis and anti-basement membrane nephritis. Immune complex nephritis is due to circulating antigen and the corresponding antibodies to form immune complexes, deposition in the glomerular basement membrane, activation of complement causing glomerular basement membrane injury, due to increased permeability, the immune complex deposition to the kidney The basement membrane of the basal lamina outside of the subcutaneous process