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Membranous nephropathy — the most common cause of nephrotic syndrome in adults. The PLA2R antibody discovery, secondary causes, and modern treatment.
Evidence reviewed & updated: 2026-08 — reflects the latest published trials and guidelines.
Membranous nephropathy is the most common cause of nephrotic syndrome in adults — immune deposits thicken the glomerular filter, leaking protein. The discovery of PLA2R antibodies made it the first autoimmune kidney disease with a defined antigen; it's now treatable with rituximab and other immunosuppression, and about a third remit spontaneously.
Membranous nephropathy is caused by immune complexes depositing along the glomerular basement membrane — the filter thickens ('membranous'), protein leaks, and nephrotic syndrome develops: heavy proteinuria, edema, low albumin, high cholesterol.
In ~70% of primary cases, autoantibodies against PLA2R (phospholipase A2 receptor) on the podocyte drive the disease — a discovery that made membranous nephropathy the first autoimmune kidney disease with a defined target antigen. Antibody levels track disease activity.
Primary membranous is autoimmune — treat the immune system. Secondary forms (~20-25%) are caused by: solid cancers (especially in older adults — malignancy screening is part of the workup), hepatitis B/C, lupus, sarcoidosis, and drugs including NSAIDs, gold, penicillamine, and some TNF inhibitors.
The workup distinguishes them: PLA2R antibody positivity strongly suggests primary; negative PLA2R in an older patient raises the cancer question; biopsy plus a careful secondary-cause screen is standard.
Low-risk patients (proteinuria <4-5 g/day, normal albumin) often get a watch-and-monitor period since ~1/3 remit spontaneously. Moderate-high risk: rituximab (now first-line in many centers), cyclophosphamide + steroids, or calcineurin inhibitors — chosen by kidney function, side-effect profile, and antibody response.
Clotting risk is real: nephrotic-range proteinuria raises thrombosis risk several-fold, and renal vein thrombosis is a classic complication — anticoagulation is considered when albumin is very low. With modern treatment, ~70-80% of patients achieve remission, and outcomes have improved substantially.
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