Membranous Nephropathy (MN) Clinical Trials and Treatments

Membranous nephropathy (MN) is an antibody-mediated glomerular disease in which IgG autoantibodies bind to antigens on the outer (subepithelial) side of the glomerular basement membrane, forming immune complexes that activate complement and thicken the filtration barrier. In about 70-80% of primary cases, the antibodies target the M-type phospholipase A2 receptor (PLA2R) on podocytes; another ~3-5% target thrombospondin type-1 domain-containing 7A (THSD7A). Other recently identified antigens (NELL-1, semaphorin-3B, exostosin) account for smaller subsets.

The most common symptoms of Membranous Nephropathy include Heavy protein in the urine (foamy urine, proteinuria), Swelling in the legs, ankles, and around the eyes (edema), Weight gain from fluid retention, High blood pressure, Increased cholesterol and triglycerides, among others. About 12 new cases per million people each year in the U.S.; roughly 40,000-50,000 Americans living with the disease. Symptoms can range from mild to severe and may vary between individuals.

Trial Friend lists all active clinical trials for Membranous Nephropathy from ClinicalTrials.gov, with eligibility criteria translated into plain English. Patients can filter by trial phase and recruitment status, search by location, and use the Match Me tool to score trials against their profile. Membranous nephropathy care is shifting from broad immunosuppression toward precision approaches that target the specific autoantibodies driving the disease. Clinical trials are testing next-generation B-cell-depleting antibodies, complement inhibitors, and investigational autoantibody degraders like Biohaven's BHV-1420, which is designed to selectively remove anti-PLA2R IgG while leaving the rest of the immune system intact.

As of September 2026, Trial Friend's curated drug index does not include an FDA-approved treatment specific to Membranous Nephropathy. The Treatments section of this page checks FDA drug labels live and lists any approved drug whose label names the condition, and the trials listed below cover the investigational options.

The exact cause of Membranous Nephropathy is not fully understood. It is not caused by a single gene; inherited variants raise risk, and immune, environmental or other triggers are thought to set it off. Primary MN is autoimmune (anti-PLA2R antibodies in 70 to 80% of cases); HLA-DQA1 variants raise risk but there is no diagnostic gene test. About 12 new cases per million people each year in the U.S.; roughly 40,000-50,000 Americans living with the disease. Research is ongoing to better understand the disease mechanism.

No single gene test diagnoses Membranous Nephropathy. The diagnosis rests on clinical findings and laboratory or imaging results; genetic variants shift risk rather than cause the disease. Primary MN is autoimmune (anti-PLA2R antibodies in 70 to 80% of cases); HLA-DQA1 variants raise risk but there is no diagnostic gene test.

Some trials collect genetic samples for research or check specific risk markers. The Genetic Testing section of this page shows any tests listed in the NIH Genetic Testing Registry, which for this condition are usually research or risk-marker tests rather than diagnostic ones.

Eligibility for Membranous Nephropathy clinical trials depends on factors like age, diagnosis, treatment history, and overall health. Each trial sets its own inclusion and exclusion criteria. Trial Friend translates these requirements from medical language into plain English so patients can review them more easily. The Match Me tool can score your profile against active trials to help identify studies that may be a fit.

Participating in a Membranous Nephropathy clinical trial typically involves scheduled visits, medical tests, and close monitoring by a research team. Depending on the study phase, you may receive an investigational treatment, a placebo, or the current standard of care. Trials may last from a few weeks to several years. Study participation is voluntary, and you can withdraw at any time.