Antiphospholipase 2 receptor antibody levels to predict complete spontaneous remission in primary membranous nephropathy

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Abstract

M-type phospholipase A2 receptor (APLA2R) is considered the major antigen involved in the pathogenesis of adult primary membranous nephropathy (MN), which is the leading cause of non-diabetic nephrotic syndrome. Antibodies to this antigen have been proved to be an excellent biomarker of disease activity in primary MN. In fact, preliminary data suggest that the higher the antibody level the more proteinuria, and that a decrease in antibody level precedes the remission of proteinuria, but more solid evidence is needed. Methods: The present work aims to characterize the predictive value of the level of antibodies against PLA2R as a biomarker of disease course and treatment response in a well-defined cohort of 62 patients from University Hospitals Clinic of Barcelona and Josep Trueta in Girona. The primary outcome was the appearance of a spontaneous complete remission (CR), defined as induction of a CR without the use of immunosuppressive agents. Results: In common with other reports, this work confirms that spontaneous CR is more frequent in patients with low titre of APLA2R at diagnosis, but strikingly, in this cohort we found that spontaneous CR was achieved in patients with APLA2R levels<40 UI/mL. Furthermore, spontaneous CR were less frequently observed in patients with proteinuria>8 g/day. Conclusions: In conclusion, these findings point out the important role of APLA2R as a tool to predict the disease course and establish personalized therapeutic options at the moment of diagnosis of primary MN. Specifically, patients with low titre of APLA2R (<40 UI/mL) and proteinuria<4/day could obtain benefit of a longer period of follow-up with conservative treatment after diagnosis.

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Rodas, L. M., Matas-García, A., Barros, X., Blasco, M., Viñas, O., Llobell, A., … Quintana, L. F. (2019). Antiphospholipase 2 receptor antibody levels to predict complete spontaneous remission in primary membranous nephropathy. Clinical Kidney Journal, 12(1), 36–41. https://doi.org/10.1093/ckj/sfy005

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