eligibility_summary
Incl: 18–75, pMN (biopsy ≤5y or anti‑PLA2R ≥14), UPCR ≥4–8 g/g with low albumin despite ACEi/ARB, eGFR ≥40. Excl: secondary MN, diabetes, eGFR <40/dialysis/transplant, ≥50% fall in proteinuria/anti‑PLA2R (6 mo), pregnancy/no contraception, recent steroids/MMF/CNI, biologics/alkylators, investigational/live vaccines, active infection (HIV, HBV/HCV+, active TB) or cancer, cytopenias, AST/ALT >2.5×ULN, HbA1c ≥6.5%. Latent TB/HBcAb+ OK with prophylaxis/monitoring, SGLT2i/GLP‑1/MRA OK if stable ≥30 d.
trial_source
clinical_trials.gov from Dec 2, 2025
annotation_status
ai
ai_summary
Phase III, randomized, open-label trial in primary membranous nephropathy comparing: 1) Obinutuzumab—type II, glycoengineered anti-CD20 IgG1 monoclonal antibody (IV at weeks 0, 2, 24, 26), mechanism: potent depletion of CD20+ B cells via ADCC/ADCP and direct cell death, reducing anti-PLA2R autoantibodies. 2) Cyclical cyclophosphamide—oral alkylating (nitrogen mustard) agent—plus glucocorticoids (IV methylprednisolone pulses, then oral prednisone), mechanisms: cyclophosphamide DNA crosslinking causes cytotoxic immunosuppression of proliferating B and T cells, glucocorticoids act via the glucocorticoid receptor to suppress NF-κB/cytokine signaling and lymphocyte function. Targets/pathways: CD20+ B cells and B-cell lineage driving humoral anti-PLA2R autoimmunity, T-cell proliferation, inflammatory transcriptional programs, and downstream immune-complex/complement-mediated podocyte injury.