Hebert L A
Department of Medicine, Ohio State University, Columbus 43220.
Am J Kidney Dis. 1988 Nov;12(5):388-92. doi: 10.1016/s0272-6386(88)80031-3.
Two fundamentally different mechanisms may account for the glomerular immune deposits in IgA nephropathy (IgAN): (1) deposition of circulating immune complexes and (2) the in situ formation of immune complexes. In this review the experimental evidence for and against an important role of circulating IgA-containing immune complexes in the pathogenesis of IgAN is summarized. Several physical characteristics, including size, lattice composition, and electrical charge, may influence the deposition of immune complexes in the renal mesangium. Furthermore, the likelihood of deposition of circulating IgA-containing immune complexes in vulnerable locations (such as the kidney) may be increased because of their impaired removal from the circulation by macrophages of the liver and spleen and the erythrocyte-immune complex clearing mechanism. However, the relative contributions of these factors to the pathogenesis of IgAN remain speculative.
两种根本不同的机制可能解释IgA肾病（IgAN）中的肾小球免疫沉积物：（1）循环免疫复合物的沉积和（2）免疫复合物的原位形成。在本综述中，总结了支持和反对循环含IgA免疫复合物在IgAN发病机制中起重要作用的实验证据。包括大小、晶格组成和电荷在内的几个物理特征可能影响免疫复合物在肾系膜中的沉积。此外，由于肝脏和脾脏的巨噬细胞以及红细胞免疫复合物清除机制对其从循环中的清除受损，循环含IgA免疫复合物在易损部位（如肾脏）沉积的可能性可能会增加。然而，这些因素在IgAN发病机制中的相对作用仍具有推测性。
