Successful treatment of PLA 2 R1-antibody positive membranous nephropathy with ocrelizumab
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CASE REPORT
Successful treatment of PLA2R1‑antibody positive membranous nephropathy with ocrelizumab Tilman Schmidt1 · Matthias Schulze2 · Sigrid Harendza1 · Elion Hoxha1 Received: 20 July 2020 / Accepted: 23 September 2020 © The Author(s) 2020
Abstract Membranous nephropathy (MN) is a common cause of nephrotic syndrome in adults. The disease is induced by antibodies, which are directed against the podocyte protein phospholipase A 2 receptor 1 (PLA2R1-ab) in 80% of cases. B cell depleting treatments, most notably rituximab, a chimeric CD20-antibody, are often effective for treatment of MN. However, in 35–40% of patients rituximab fails to induce remission of disease and relapses after rituximab-induced remission are frequent. Therefore, alternative treatment options are necessary. Over the past years optimized antibodies targeting CD20 were designed to overcome side effects or sensitization to the murine fractions of rituximab and potentially improve B cell depletion. Ocrelizumab is a humanized B cell depleting antibody, approved for treatment of multiple sclerosis (MS). Here, we report the case of a patient who was diagnosed with MS and, 8 years later, developed P LA2R1-associated MN. Treatment for MS was switched to the CD20-antibody ocrelizumab, which was expected to deplete B cells and potentially induce remission of MN. After treatment with ocrelizumab PLA2R1-ab disappeared from the circulation and the patient developed remission of proteinuria. Ocrelizumab might be an efficacious treatment alternative for patients with MN who fail to achieve remission or are immunologically sensitized to rituximab. Keywords Membranous nephropathy · Rituximab · Ocrelizumab · Nephrotic syndrome
Introduction Membranous nephropathy (MN) is an autoimmune disease and a common cause of nephrotic syndrome in adults. MN has been associated with different disease conditions, e.g. chronic infections (hepatitis B), malignancies, or different autoimmune diseases in up to 25% of cases, which are then considered secondary [1]. Phospholipase A 2 receptor 1 (PLA2R1) is the major target antigen in MN and up to 80% of patients have circulating antibodies directed against this protein [2]. Autoantibody binding leads to formation of Electronic supplementary material The online version of this article (https://doi.org/10.1007/s40620-020-00874-2) contains supplementary material, which is available to authorized users. * Elion Hoxha [email protected] 1
III. Department of Internal Medicine, University Medical Center Hamburg-Eppendorf, Martinistr. 52, 20246 Hamburg, Germany
Viamedis Renal Center Bad Zwischenahn, Bad Zwischenahn, Germany
2
immune deposits on the glomerular basement membrane, ultimately causing nephrotic syndrome due to loss of proteins in the urine. In the long term, about one-third of patients will achieve spontaneous remission of proteinuria, especially patients with low P LA2R1-antibody level [3–5]. At the same time, approximately 16% of patients with MN develop end-stage renal disease over 5–10 years [3].
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