The anti-PLA2R antibody test detects autoantibodies against the phospholipase A2 receptor in blood, primarily used to diagnose and monitor primary membranous nephropathy. Positive or high levels support an autoimmune cause, guide treatment decisions, predict disease activity and prognosis, and track response or relapse during therapy. It can also reduce the need for invasive kidney biopsy in some cases.

A positive phospholipase A2 receptor (PLA2R) antibody test usually indicates autoimmune (primary) membranous nephropathy, a kidney disease that can cause nephrotic-range proteinuria. It reflects antibodies targeting podocytes, supports diagnosis, helps distinguish primary from secondary causes, and often correlates with disease activity and prognosis. Levels can guide treatment and monitoring but are interpreted with clinical and biopsy findings.

The anti‑PLA2R (serum) test typically costs roughly US$20–400 depending on country, lab, and whether public healthcare or insurance covers it. In lower‑cost markets (e.g., India) it’s often INR ~1,500–5,000 (~US$20–65); in private U.S. labs it commonly ranges US$100–400. Check with your local lab or insurer for exact pricing and coverage.

Primary membranous nephropathy is an autoimmune kidney disease caused by autoantibodies against the M-type phospholipase A2 receptor (PLA2R) on podocytes. Anti-PLA2R antibodies form immune complexes that injure the glomerular basement membrane, leading to heavy proteinuria and nephrotic syndrome. Measuring anti-PLA2R antibodies aids diagnosis, monitoring, and distinguishing primary from secondary membranous nephropathy.

If anti-PLA2R is negative, PLA2R-associated primary membranous nephropathy is less likely. Further evaluation—kidney biopsy and testing for other target antigens (e.g., THSD7A, NELL1) and screening for secondary causes (autoimmune disease, infection, malignancy, drugs)—is recommended. Management focuses on treating the underlying cause, controlling proteinuria and blood pressure, and considering immunosuppression for persistent severe disease.

Treat membranous nephropathy by controlling blood pressure and reducing proteinuria with ACE inhibitors or ARBs; manage edema with diuretics and salt restriction; treat lipids with statins; assess thrombotic risk and consider anticoagulation if indicated. Immunosuppressive therapy (rituximab, calcineurin inhibitors, or cyclophosphamide plus steroids) is used for persistent nephrotic syndrome or declining renal function. Regular specialist follow-up is essential.