{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,9]],"date-time":"2026-11-09T15:04:25Z","timestamp":1794236665487,"version":"4.9.0"},"reference-count":66,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["JASN"],"published-print":{"date-parts":[[2017,2]]},"abstract":"<jats:p>Primary membranous nephropathy (MN) is an autoimmune disease mainly caused by autoantibodies against the recently discovered podocyte antigens: the M-type phospholipase A2 receptor 1 (PLA2R) and thrombospondin type 1 domain-containing 7A (THSD7A). Assays for quantitative assessment of anti-PLA2R antibodies are commercially available, but a semiquantitative test to detect anti-THSD7A antibodies has been only recently developed. The presence or absence of anti-PLA2R and anti-THSD7A antibodies adds important information to clinical and immunopathologic data in discriminating between primary and secondary MN. Levels of anti-PLA2R antibodies and possibly, anti-THSD7A antibodies tightly correlate with disease activity. Low baseline and decreasing anti-PLA2R antibody levels strongly predict spontaneous remission, thus favoring conservative therapy. Conversely, high baseline or increasing anti-PLA2R antibody levels associate with nephrotic syndrome and progressive loss of kidney function, thereby encouraging prompt initiation of immunosuppressive therapy. Serum anti-PLA2R antibody profiles reliably predict response to therapy, and levels at completion of therapy may forecast long-term outcome. Re-emergence of or increase in antibody titers precedes a clinical relapse. Persistence or reappearance of anti-PLA2R antibodies after kidney transplant predicts development of recurrent disease. We propose that an individualized serology-based approach to MN, used to complement and refine the traditional proteinuria-driven approach, will improve the outcome in this disease.<\/jats:p>","DOI":"10.1681\/asn.2016070776","type":"journal-article","created":{"date-parts":[[2016,10,24]],"date-time":"2016-10-24T22:29:52Z","timestamp":1477348192000},"page":"421-430","source":"Crossref","is-referenced-by-count":327,"title":["A Proposal for a Serology-Based Approach to Membranous Nephropathy"],"prefix":"10.1681","volume":"28","author":[{"given":"An S.","family":"De Vriese","sequence":"first","affiliation":[{"name":"Division of Nephrology, AZ Sint-Jan Brugge-Oostende, Brugge, Belgium;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Richard J.","family":"Glassock","sequence":"additional","affiliation":[{"name":"Department of Medicine, Geffen School of Medicine, University of California, Los Angeles, California; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Karl A.","family":"Nath","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Hypertension and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sanjeev","family":"Sethi","sequence":"additional","affiliation":[{"name":"Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, Minnesota"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fernando C.","family":"Fervenza","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Hypertension and"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","published-online":{"date-parts":[[2016,10,24]]},"reference":[{"key":"B1-20231016","doi-asserted-by":"crossref","first-page":"11","DOI":"10.1056\/NEJMoa0810457","article-title":"M-type phospholipase A2 receptor as target antigen in idiopathic membranous nephropathy.","volume":"361","author":"Beck","year":"2009","journal-title":"N 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