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许多免疫性肾疾患是抗原抗体复合物沉着于肾小球毛细血管壁所致,但免疫复合物沉着的具体机理未明。一般认为,免疫复合物随血流到达肾小球时,由于滤过作用而被动地沉着于毛细血管壁上,因而肾小球毛细血管襻对于免疫复合物的沉着起相对的非特异性作用。作者最近发现正常人肾脏的肾小球有特异性的,只和补体C_3结合的受体,从而提出了这样的一种可能:即是免疫复合物所致的肾疾患的发病机理是含有C_3的免疫复合物被肾小球毛细血管壁的补体受体所结合,沉着在肾小球所引起的,这样,免疫复合物的沉着也可以说是有一定的特异性。为了探讨上述设想是否合乎实际,本文采取各种肾疾患的活检标本,研究肾小球是否有免疫球蛋白和补体沉着,以及肾小
Many autoimmune kidney disorders are caused by the deposition of antigen-antibody complexes on the glomerular capillary walls, but the exact mechanism of immune complex deposition is unknown. It is generally believed that when the immune complexes reach the glomerulus with blood flow, they passively settle on the walls of the capillaries due to filtration and thus glomerular capillaries play a relatively non-specific role in the calming of immune complexes. The authors have recently found that glomeruli in normal human kidneys have a specific receptor that binds only to complement C_3, thereby raising the possibility that the pathogenesis of immune complex-induced nephropathy is C_3-containing Immune complexes by the glomerular capillary wall complement receptor binding, caused by deposition in the glomerular, so immune complex deposition can also be said that there is a certain specificity. In order to explore whether these ideas are realistic, this article to take a variety of kidney disease biopsy specimens to study whether glomerular immunoglobulin and complement deposition, and kidney