Oliveira D B G
Department of Renal Medicine, St. George's Hospital Medical School, Cranmer Terrace, London, United Kingdom.
Minerva Med. 2002 Oct;93(5):323-8.
Membranous nephropathy is an important disease: it is one of the leading primary causes of the nephrotic syndrome in adults, and, in up to a third of patients, causes progressive renal impairment resulting in end stage renal failure. Ever since histological techniques demonstrated the presence of glomerular immunoglobulin deposits in this disease the immune system has been implicated in pathogenesis. Initial ideas focussed on the deposition of circulating immune complexes, but the development of an animal model (Heymann nephritis) suggested the alternative mechanism of antibody reacting with an intrinsic glomerular antigen. However, attempts to find evidence for this Heymann type mechanism in the human disease have, in general, been unsuccessful. This article briefly reviews the development of ideas about the pathogenesis of membranous nephropathy, and proposes the hypothesis that the disease is caused by formation of low affinity non-complement fixing IgG4-containing immune complexes.
它是成人肾病综合征的主要原发性病因之一，在多达三分之一的患者中，会导致进行性肾功能损害，最终发展为终末期肾衰竭。自从组织学技术证实该疾病中存在肾小球免疫球蛋白沉积以来，免疫系统就被认为与发病机制有关。最初的观点集中在循环免疫复合物的沉积上，但动物模型（海曼肾炎）的发展提示了抗体与内源性肾小球抗原反应的另一种机制。然而，总体而言，在人类疾病中寻找这种海曼型机制证据的尝试并不成功。本文简要回顾了关于膜性肾病发病机制观点的发展，并提出该疾病是由含低亲和力、非补体结合的IgG4免疫复合物形成所致的假说。
