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IgA 肾病发病机制的分子见解。

Molecular Insights into the Pathogenesis of IgA Nephropathy.

机构信息

Department of Nephrology Transplantation and Emergency, Assistance Publique-Hôpitaux de Paris, Tenon Hospital, Paris, France; University Pierre et Marie Curie Paris 6, Paris, France.

Institut National de la Santé et de la Recherche Médicale (INSERM) Unité 1149, Center for Research on Inflammation, Centre National de la Recherche Scientifique (CNRS) Equipe de Recherche Labellisée 8252, Paris, France; University Paris Diderot, Paris 7, Inflamex Laboratory of Excellence, Site Xavier Bichat, Paris, France.

出版信息

Trends Mol Med. 2015 Dec;21(12):762-775. doi: 10.1016/j.molmed.2015.10.003. Epub 2015 Nov 21.

DOI:10.1016/j.molmed.2015.10.003
PMID:26614735
Abstract

Immunoglobulin IgA nephropathy (IgAN) is the leading form of primary glomerulonephritis associated with end-stage renal failure, requiring either dialysis or renal transplantation. Microscopic hematuria and proteinuria are the most common presentations, and mesangial cell proliferation with IgA deposition are found in renal biopsies. There is growing evidence that IgAN is an immune complex (IC)-mediated disease. To date, three key molecules have been implicated in IC formation, correlating with disease progression/recurrence after transplantation: galactose-deficient IgA1 (Gd-IgA1), IgG anti-Gd-IgA1 antibodies, and soluble CD89 (an Fc receptor for IgA). This review examines recent data on the role of these molecular players in IgAN. Understanding these factors is essential because such knowledge could lead to improved strategies for the future management of patients with IgAN.

摘要

免疫球蛋白 A 肾病(IgAN)是导致终末期肾衰竭的主要原发性肾小球肾炎形式,需要透析或肾移植。血尿和蛋白尿是最常见的表现,肾活检中发现系膜细胞增殖和 IgA 沉积。越来越多的证据表明 IgAN 是一种免疫复合物(IC)介导的疾病。迄今为止,有三个关键分子与 IC 形成相关,与移植后疾病进展/复发相关:半乳糖缺乏 IgA1(Gd-IgA1)、IgG 抗 Gd-IgA1 抗体和可溶性 CD89(IgA 的 Fc 受体)。本文综述了这些分子在 IgAN 中的作用的最新数据。了解这些因素至关重要,因为这些知识可能会导致未来改善 IgAN 患者管理的策略。

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