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Idiopathic Membranous Nephropathy: Glomerular Pathological Pattern Caused by Extrarenal Immunity Activity

Idiopathic membranous nephropathy (IMN) is a pathological pattern of glomerular damage caused by an autoimmune response. Immune complex deposition, thickness of glomerular basement membrane, and changes in the podocyte morphology are responsible for the development of proteinuria, which is caused by...

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Autores principales: Liu, Wenbin, Gao, Chang, Liu, Zhiyuan, Dai, Haoran, Feng, Zhendong, Dong, Zhaocheng, Zheng, Yang, Gao, Yu, Tian, Xuefei, Liu, Baoli
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7524879/
https://www.ncbi.nlm.nih.gov/pubmed/33042109
http://dx.doi.org/10.3389/fimmu.2020.01846
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author Liu, Wenbin
Gao, Chang
Liu, Zhiyuan
Dai, Haoran
Feng, Zhendong
Dong, Zhaocheng
Zheng, Yang
Gao, Yu
Tian, Xuefei
Liu, Baoli
author_facet Liu, Wenbin
Gao, Chang
Liu, Zhiyuan
Dai, Haoran
Feng, Zhendong
Dong, Zhaocheng
Zheng, Yang
Gao, Yu
Tian, Xuefei
Liu, Baoli
author_sort Liu, Wenbin
collection PubMed
description Idiopathic membranous nephropathy (IMN) is a pathological pattern of glomerular damage caused by an autoimmune response. Immune complex deposition, thickness of glomerular basement membrane, and changes in the podocyte morphology are responsible for the development of proteinuria, which is caused by the targeted binding of auto-antibodies to podocytes. Several auto-antigens have recently been identified in IMN, including M-type receptor for secretory phospholipase A2 (PLA2R1), thrombospondin type-1 domain-containing 7A (THSD7A), and neural epidermal growth factor-like 1 protein (NELL-1). The measurement of peripheral circulating antibodies has become an important clinical reference index. However, some clinical features of IMN remain elusive and need to be further investigated, such as the autoimmunity initiation, IgG4 predominance, spontaneous remission, and the unique glomerular lesion. As these unresolved issues are closely related to clinical practice, we have proposed a hypothetical pathogenesis model of IMN. Induced by environmental stimuli or other causes, the PLA2R1 antigen and/or THSD7A antigen exposed to extrarenal tissues, such as lungs, then produce the auto-antibodies that target and cause damage to the podocytes in circulation. In this review, we highlighted the potential association between environmental stimuli, immune activity, and glomerular lesions, the underlying basis for spontaneous immune and proteinuria remission.
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spelling pubmed-75248792020-10-09 Idiopathic Membranous Nephropathy: Glomerular Pathological Pattern Caused by Extrarenal Immunity Activity Liu, Wenbin Gao, Chang Liu, Zhiyuan Dai, Haoran Feng, Zhendong Dong, Zhaocheng Zheng, Yang Gao, Yu Tian, Xuefei Liu, Baoli Front Immunol Immunology Idiopathic membranous nephropathy (IMN) is a pathological pattern of glomerular damage caused by an autoimmune response. Immune complex deposition, thickness of glomerular basement membrane, and changes in the podocyte morphology are responsible for the development of proteinuria, which is caused by the targeted binding of auto-antibodies to podocytes. Several auto-antigens have recently been identified in IMN, including M-type receptor for secretory phospholipase A2 (PLA2R1), thrombospondin type-1 domain-containing 7A (THSD7A), and neural epidermal growth factor-like 1 protein (NELL-1). The measurement of peripheral circulating antibodies has become an important clinical reference index. However, some clinical features of IMN remain elusive and need to be further investigated, such as the autoimmunity initiation, IgG4 predominance, spontaneous remission, and the unique glomerular lesion. As these unresolved issues are closely related to clinical practice, we have proposed a hypothetical pathogenesis model of IMN. Induced by environmental stimuli or other causes, the PLA2R1 antigen and/or THSD7A antigen exposed to extrarenal tissues, such as lungs, then produce the auto-antibodies that target and cause damage to the podocytes in circulation. In this review, we highlighted the potential association between environmental stimuli, immune activity, and glomerular lesions, the underlying basis for spontaneous immune and proteinuria remission. Frontiers Media S.A. 2020-09-16 /pmc/articles/PMC7524879/ /pubmed/33042109 http://dx.doi.org/10.3389/fimmu.2020.01846 Text en Copyright © 2020 Liu, Gao, Liu, Dai, Feng, Dong, Zheng, Gao, Tian and Liu. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Immunology
Liu, Wenbin
Gao, Chang
Liu, Zhiyuan
Dai, Haoran
Feng, Zhendong
Dong, Zhaocheng
Zheng, Yang
Gao, Yu
Tian, Xuefei
Liu, Baoli
Idiopathic Membranous Nephropathy: Glomerular Pathological Pattern Caused by Extrarenal Immunity Activity
title Idiopathic Membranous Nephropathy: Glomerular Pathological Pattern Caused by Extrarenal Immunity Activity
title_full Idiopathic Membranous Nephropathy: Glomerular Pathological Pattern Caused by Extrarenal Immunity Activity
title_fullStr Idiopathic Membranous Nephropathy: Glomerular Pathological Pattern Caused by Extrarenal Immunity Activity
title_full_unstemmed Idiopathic Membranous Nephropathy: Glomerular Pathological Pattern Caused by Extrarenal Immunity Activity
title_short Idiopathic Membranous Nephropathy: Glomerular Pathological Pattern Caused by Extrarenal Immunity Activity
title_sort idiopathic membranous nephropathy: glomerular pathological pattern caused by extrarenal immunity activity
topic Immunology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7524879/
https://www.ncbi.nlm.nih.gov/pubmed/33042109
http://dx.doi.org/10.3389/fimmu.2020.01846
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