title: [Treatment of idiopathic membranous nephropathy. Is the anti-CD20 antibody rituximab a reasonable option?].
abstract: BACKGROUND
  Membranous nephropathy (MN) is characterized by proteinuria and other symptoms of the nephrotic syndrome. In many cases, the etiology is unknown. Whether and how to treat MN is still a controversial question. Despite the use of corticosteroids and alkylating agents, up to 40% of patients still progress to end-stage renal failure.
  
  
  METHODS
  A 40-year-old male patient with biopsy-proven idiopathic MN was initially treated with prednisolone and chlorambucil because of a proteinuria of 22 g/d. Treatment with cyclosporine was started because the nephrotic syndrome failed to improve. Proteinuria was reduced to a minimum of 4 g/d. Cyclosporine was stopped after 17 months leading to a fast relapse. Therapy with an ACE inhibitor and AT(1) receptor antagonist and retreatment with cyclosporine improved proteinuria. Cyclosporine was terminated after a total of 24 months. 5 months later, relapse occurred with a high proteinuria of 34 g/d. The monoclonal anti-CD20 antibody rituximab (375 mg/m(2)) was given four times every 4 weeks. 4 weeks and 4 months after the end of treatment, proteinuria decreased to 780 mg/d and <150 mg/d, but renal function remained impaired (creatinine clearance 65 ml/min, stage 2 according to K/DOQI). Now, remission of proteinuria (<150 mg/d) has been stable for almost 2 years. However, renal insufficiency progressed further (creatinine clearance 45 ml/min, stage 3 according to K/DOQI).
  
  
  CONCLUSIONS
  Rituximab offers the possibility for a targeted treatment of idiopathic MN. Based on the existing evidence and experience from this case, rituximab can be recommended as a new treatment option for MN, possibly before starting any treatment with cytotoxic agents and high-dose prednisolone carrying the risk of severe side effects. However, long-term results of this treatment are still lacking.
authors.affiliation: Klinik für Innere Medizin III, Klinikum der Friedrich-Schiller-Universität Jena, Jena. martin.busch@med.uni-jena.de
authors.forename: Martin
authors.initials: M
authors.lastname: Busch
authors.forename: Jens
authors.initials: J
authors.lastname: Gerth
authors.forename: Undine
authors.initials: U
authors.lastname: Ott
authors.forename: Andre
authors.initials: A
authors.lastname: Schip
authors.forename: Christoph C
authors.initials: CC
authors.lastname: Haufe
authors.forename: Hermann-Josef
authors.initials: HJ
authors.lastname: Gröne
authors.forename: Gunter
authors.initials: G
authors.lastname: Wolf
mesh_terms: D000328:Adult; D000911:Antibodies, Monoclonal / Q000009:adverse effects / Q000627:therapeutic use*; D058846:Antibodies, Monoclonal, Murine-Derived; D001706:Biopsy; D004351:Drug Resistance; D004359:Drug Therapy, Combination; D050533:Glomerular Basement Membrane / Q000473:pathology; D015433:Glomerulonephritis, Membranous / Q000175:diagnosis / Q000188:drug therapy* / Q000209:etiology / Q000473:pathology; D006801:Humans; D007070:Immunoglobulin A; D007155:Immunologic Factors / Q000009:adverse effects / Q000627:therapeutic use*; D007166:Immunosuppressive Agents / Q000009:adverse effects / Q000627:therapeutic use; D007677:Kidney Function Tests; D007678:Kidney Glomerulus / Q000473:pathology; D008297:Male; D000069283:Rituximab
chemical_list: D000911:Antibodies, Monoclonal; D058846:Antibodies, Monoclonal, Murine-Derived; D007070:Immunoglobulin A; D007155:Immunologic Factors; D007166:Immunosuppressive Agents; D000069283:Rituximab