title: B cell suppression in primary glomerular disease.
abstract: Membranous nephropathy, focal segmental glomerulosclerosis (FSGS), and minimal change disease (MCD) are the most common causes of idiopathic nephrotic syndrome. For many years prednisone, alkylating agents, and calcineurin inhibitors have been the standard of therapy for these patients. More effective or better tolerated treatment modalities are needed. B cell targeted therapy was recently introduced in clinical practice. In this review, we briefly summarize the current standard therapy and discuss the efficacy of B cell targeted therapy in primary glomerular diseases. Observational, short-term studies suggest that rituximab is effective and comparable to standard therapy in maintaining remissions in patients with frequently relapsing or steroid-dependent MCD or FSGS. In contrast, response is limited in patients with steroid-resistant nephrotic syndrome. Rituximab also induces remissions in patients with membranous nephropathy. Controlled clinical trials on kidney endpoints are urgently needed to position B cell targeted therapy in clinical practice.
authors.affiliation: Department of Nephrology, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands. Electronic address: ilse.rood@radboudumc.nl.
authors.forename: Ilse M
authors.initials: IM
authors.lastname: Rood
authors.affiliation: Department of Nephrology, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands.
authors.forename: Julia M
authors.initials: JM
authors.lastname: Hofstra
authors.affiliation: Department of Nephrology, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands.
authors.forename: Jeroen K J
authors.initials: JK
authors.lastname: Deegens
authors.affiliation: Department of Nephrology, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands.
authors.forename: Jack F M
authors.initials: JF
authors.lastname: Wetzels
mesh_terms: D000069594:Abatacept; D061067:Antibodies, Monoclonal, Humanized / Q000627:therapeutic use; D058846:Antibodies, Monoclonal, Murine-Derived / Q000627:therapeutic use; D001402:B-Lymphocytes / Q000276:immunology*; D005921:Glomerulonephritis / Q000188:drug therapy / Q000276:immunology; D015433:Glomerulonephritis, Membranous / Q000188:drug therapy* / Q000276:immunology; D005923:Glomerulosclerosis, Focal Segmental / Q000188:drug therapy* / Q000276:immunology; D006801:Humans; D018796:Immunoconjugates / Q000627:therapeutic use; D007166:Immunosuppressive Agents / Q000627:therapeutic use*; D009402:Nephrosis, Lipoid / Q000188:drug therapy* / Q000276:immunology; D009841:Oligonucleotides / Q000627:therapeutic use; D011241:Prednisone / Q000627:therapeutic use; D011993:Recombinant Fusion Proteins / Q000627:therapeutic use; D000069283:Rituximab
chemical_list: D061067:Antibodies, Monoclonal, Humanized; D058846:Antibodies, Monoclonal, Murine-Derived; D018796:Immunoconjugates; D007166:Immunosuppressive Agents; D009841:Oligonucleotides; D011993:Recombinant Fusion Proteins; C448700:epratuzumab; D000069283:Rituximab; C511911:belimumab; D000069594:Abatacept; C533411:ocrelizumab; C524618:TACI receptor-IgG Fc fragment fusion protein; C094104:abetimus; D011241:Prednisone
keywords: Focal segmental glomerulosclerosis; Membranous nephropathy; Minimal change disease; Rituximab