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BioMed Research International
Volume 2018, Article ID 6281054, 19 pages
Review Article

Membranous Nephropathy and Anti-Podocytes Antibodies: Implications for the Diagnostic Workup and Disease Management

1Nephrology Department, Centre Hospitalier Universitaire de Bruxelles (CHUB), Brugmann Hospital, Brussels, Belgium
2Université Libre de Bruxelles (ULB), Brussels, Belgium
3Pathology Department, AP-HP, Pitié Hospital, Paris, France
4UPMC Université Paris 6, Paris, France
5Centre National de Référence Maladies Rares: Amylose AL et Autres Maladies à Dépôts d’Immunoglobulines Monoclonales, Université de Poitiers, Poitiers, France
6Pathology Department, Centre Hospitalier Universitaire de Poitiers, Poitiers, France
7Nephrology Department, Universitair Ziekenhuis Brussel, Vrije Universiteit Brussel, Brussels, Belgium

Correspondence should be addressed to Agnieszka Pozdzik; eb.nnamgurb-uhc@kizdzop.akzseinga

Received 11 June 2017; Revised 31 August 2017; Accepted 15 October 2017; Published 8 January 2018

Academic Editor: Michael Mahler

Copyright © 2018 Agnieszka Pozdzik et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The discovery of circulating antibodies specific for native podocyte antigens has transformed the diagnostic workup and greatly improved management of idiopathic membranous nephropathy (iMN). In addition, their identification has clearly characterized iMN as a largely autoimmune disorder. Anti-PLA2R1 antibodies are detected in approximately 70% to 80% and anti-THSD7A antibodies in only 2% of adult patients with iMN. The presence of anti-THSD7A antibodies is associated with increased risk of malignancy. The assessment of PLA2R1 and THSD7A antigen expression in glomerular immune deposits has a better sensitivity than measurement of the corresponding autoantibodies. Therefore, in the presence of circulating anti-podocytes autoantibodies and/or enhanced expression of PLA2R1 and THSD7A antigens MN should be considered as primary MN (pMN). Anti-PLA2R1 or anti-THSD7A autoantibodies have been proposed as biomarkers of autoimmune disease activity and their blood levels should be regularly monitored in pMN to evaluate disease activity and predict outcomes. We propose a revised clinical workup flow for patients with MN that recommends assessment of kidney biopsy for PLA2R1 and THSD7A antigen expression, screening for circulating anti-podocytes antibodies, and assessment for secondary causes, especially cancer, in patients with THSD7A antibodies. Persistence of anti-podocyte antibodies for 6 months or their increase in association with nephrotic proteinuria should lead to the introduction of immunosuppressive therapies. Recent data have reported the efficacy and safety of new specific therapies targeting B cells (anti-CD20 antibodies, inhibitors of proteasome) in pMN which should lead to an update of currently outdated treatment guidelines.