eligibility_summary
Adults 18–75, biopsy‑proven primary membranous nephropathy, after ≥3 mo ACEi/ARB (unless intolerant) and proteinuria ≥3.5 g/d twice/1 wk or ≥5 g/d twice/14 d, BP ≤130/80, eGFR ≥30, women postmenopausal/infertile or on contraception, consent. Exclude diabetic nephropathy, secondary MN, prior immunosuppressants, recent trial drug, allergy, active HBV/HCV/TB/HIV, immunodeficiency/transplant, pregnancy/lactation, mental illness, key lab cytopenias or AST/ALT>2.5×ULN, high risk, or per investigator.
trial_source
clinical_trials.gov from Dec 2, 2025
annotation_status
ai
ai_summary
NCT05514015 tests rituximab plus corticosteroids vs rituximab alone in treatment‑naïve primary membranous nephropathy. Rituximab is a chimeric anti‑CD20 monoclonal antibody that depletes CD20+ B cells via CDC/ADCC/apoptosis, lowering pathogenic autoantibodies (notably anti‑PLA2R) that drive podocyte injury and complement activation. Corticosteroids (prednisolone, dexamethasone as premed) are systemic glucocorticoids that suppress NF‑κB–mediated cytokine signaling and T‑ and B‑cell activity, broadly dampening inflammation. Targets/pathways: peripheral B cells (CD20+, monitored by CD19+ counts), anti‑PLA2R autoantibody production, podocyte PLA2R antigen–antibody axis, and downstream complement-mediated glomerular injury. Primary endpoint: 12‑month complete response, secondary includes anti‑PLA2R titers, CD19+ counts, eGFR, relapse, safety.