eligibility_summary
Includes: nephrotic syndrome with normal renal function, idiopathic membranous nephropathy confirmed by pathology, no steroid or immunosuppressive therapy in past 6 months. Excludes: inability to receive steroids/immunosuppression, prior intracranial disease (stroke/hemorrhage), cognitive decline/dementia, claustrophobia or MRI contraindications (pacemaker/metal), pregnant or breastfeeding.
trial_source
clinical_trials.gov from Dec 2, 2025
annotation_status
ai
ai_summary
Interventions: 1) Ponticelli regimen—alternating high-dose IV methylprednisolone then oral prednisone with oral cyclophosphamide, 2) Rituximab with B-cell–guided redosing. Mechanisms: Glucocorticoids (prednisone/methylprednisolone, steroidal anti-inflammatories) activate the glucocorticoid receptor to suppress NF-κB/AP-1 signaling, lowering cytokines, T-cell activity, and antibody production. Cyclophosphamide (alkylating immunosuppressant) crosslinks DNA and preferentially depletes proliferating B/T lymphocytes, reducing autoantibody generation. Rituximab (anti-CD20 monoclonal antibody) depletes CD20+ B cells via ADCC/CDC/apoptosis, decreasing anti-PLA2R autoantibodies central to idiopathic membranous nephropathy. Targets/pathways: CD20+ B cells, humoral autoimmunity, NF-κB/AP-1 inflammatory pathways, and downstream podocyte/GBM immune-complex/complement injury. The study compares cognitive effects (fMRI) of these regimens in IMN.