Membranous nephropathy is a noninflammatory autoimmune disease of the kidney glomerulus, characterized by the formation of immune deposits, complement-mediated proteinuria, and risk of renal failure. Considerable advances in understanding the molecular pathogenesis have occurred with the identification of several antigens [neutral endopeptidase, phospholipase A2 receptor (PLA2R), thrombospondin domain-containing 7A (THSD7A)] in cases arising from the neonatal period to adulthood and the characterization of antibody-binding domains (that is, epitopes). Immunization against PLA2R occurs in 70% to 80% of adult cases. The development of highly specific and sensitive assays of circulating antibodies has induced a paradigm shift in diagnosis and treatment monitoring. In addition, several interacting loci in HLA-DQ, HLA-DR, and PLA2R1, as well as classical human leukocyte antigen (HLA)-D alleles have been identified as being risk factors, depending on a patient's ethnicity. Additionally, mechanisms of antibody pathogenicity and pathways of complement activation are now better understood. Further research is mandatory for designing new therapeutic strategies, including the identifying triggering events, the molecular bases of remission and progression, and the T cell epitopes involved.

中文翻译：

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膜性肾病的分子发病机制。

膜性肾病是肾小球的一种非炎性自身免疫性疾病，其特征在于免疫沉积物的形成，补体介导的蛋白尿和肾衰竭的风险。在新生儿期到成年期间鉴定几种抗原[中性内肽酶，磷脂酶A2受体（PLA2R），含血小板反应蛋白域的7A（THSD7A）]方面，在分子发病机理的理解方面已取得了重大进展。结合结构域（即表位）。70％至80％的成年人感染PLA2R。循环抗体的高度特异性和灵敏测定方法的发展已引起诊断和治疗监测的范式转变。此外，HLA-DQ，HLA-DR和PLA2R1中有几个相互作用的基因座，根据患者的种族，人类经典白细胞抗原（HLA）-D等位基因已被确定为危险因素。另外，现在对抗体致病性的机制和补体激活的途径有了更好的了解。为了设计新的治疗策略，必须进行进一步的研究，包括确定触发事件，缓解和进展的分子基础以及所涉及的T细胞表位。