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Sir,  Anti-glomerular basement membrane (GBM) nephritis is an autoimmune disease characterized by IgG antibodyformation against the α3 (IV)NCI non-collagenous region of type IV collagen resulting in rapid progressive glomerulonephritis and, ultimately, renal failure when left untreated [1]. Several novel agents have been used when conventional therapy fails to suppress antibody formation. We describe the case of a young woman with severe anti-GBM disease who had persistently high antibody titres despite conventional therapy, experiencing successful antibody suppression after rituximab was added to her therapeutic regimen.  A 20-year-old woman presented at the emergency department with acute, oliguric renal failure due to glomerulonephritis. Creatinine level was 624 mmol/L, urea level was 16 mmol/L, and 24-h protein excretion was 6.2 g. Anti-GBM titre was positive with 270 units, while ANCA-P3/MPO and ANA were negative.  The diagnosis of anti-GBM glomerulonephritis was made, and plasmapheresis was initiated while the patient was started on methylprednisolone 1 g i.v. for 3 days followed by 1 mg/kg and cyclophosphamide 2 mg/kg, both orally.  At Day 21, after 17 sessions of plasmapheresis with 3 L plasma volumes, the anti-GBM titre remained elevated at 180 units, and proteinuria worsened to 40 g/day.  Rituximab was initiated at a dose of 375 mg/m2 with a 2-week interval. Four days after first rituximab treatment, the anti-GBM titre dropped to 130 units, and 11 days later the titre had further decreased to 85 units. Four weeks after the first dose of rituximab and 2 months after the diagnosis was made, the anti-GBM titre had dropped to below reference level, while proteinuria declined to 2 g/24 h and creatinine clearance rose to 32 (Modification of Diet in Renal Disease formula). Phenotyping of peripheral lymphocytes showed B cells to be almost completely absent.  The use of rituximab in anti-GBM nephritis has only been described in case studies, with mixed outcome, but its use has been successfully studied as adjuvant or salvage therapy in antibody-mediated autoimmune diseases such as autoimmune thrombocytopenic purpura, autoimmune haemolytic anaemia, systemic lupus erythematosus and rheumatoid arthritis. [2–4] The production of antibody depends on the antigenically driven clonal expansion of B cells into antibody-producing effector plasma cells. Plasma cells are short-lived cells, and survival of the populations depends on differentiation from their progenitor B cells [5]. B-cell ablation with rituximab could prevent further plasma cell and subsequent antibody formation, extinguishing the inflammatory anti-GBM response.  In our case, the anti-GBM titre did not decrease below reference level even though 51 L of plasma volume had been exchanged, suggesting a high rate of antibody formation. The rapid decline of antibody titre and proteinuria could very well have been due to a late effect of simultaneous earlier therapy, but the theory behind the use of rituximab does not rule out that the rituximab might have had beneficial effect on antibody formation.  Conflict of interest statement. None declared.

Additional antibody suppression from rituximab added to conventional therapy in severe, refractory anti-GBM nephritis