The anti‑PLA2R antibody test detects autoantibodies to the phospholipase A2 receptor on podocytes. It is used mainly to diagnose primary membranous nephropathy, distinguish primary from secondary causes, and monitor disease activity. Antibody levels usually correlate with proteinuria, treatment response and prognosis, helping predict relapse and guide immunosuppressive therapy, often reducing the need for repeat kidney biopsy.

PLA2R positive means a person has antibodies against the M-type phospholipase A2 receptor (or PLA2R antigen in kidney tissue), which is strongly associated with primary membranous nephropathy. It supports an autoimmune diagnosis, helps distinguish primary from secondary causes, and provides prognostic and monitoring information—higher antibody levels correlate with more active disease and greater risk of proteinuria or kidney progression.

The anti‑phospholipase A2 receptor (anti‑PLA2R) is an autoantibody targeting the PLA2R protein on podocyte surfaces in the kidney. It is a key marker of primary membranous nephropathy: blood testing for anti‑PLA2R helps diagnose and distinguish primary from secondary causes, monitor disease activity, predict prognosis, and guide treatment—higher antibody titres generally indicate more active disease.

Autoantibodies against the M-type phospholipase A2 receptor (PLA2R) cause primary membranous nephropathy, an autoimmune kidney disease that damages podocytes and produces subepithelial immune deposits. It is a common cause of nephrotic syndrome in adults; testing for anti-PLA2R antibodies helps diagnose and monitor disease activity and guide treatment decisions. Most cases are idiopathic, though some are secondary to infection, drugs, or malignancy.

If serum PLA2R antibodies are negative, membranous nephropathy may still be primary (antibodies can be tissue-restricted or against other antigens) or secondary to drugs, infections, autoimmune disease, or cancer. Next steps include repeat or tissue PLA2R testing, evaluation for secondary causes, testing for other antigens (e.g., THSD7A, NELL1), and close monitoring of proteinuria, renal function, and blood pressure.

Treat membranous nephropathy with supportive care: blood-pressure control (ACE inhibitor or ARB) to reduce proteinuria, salt restriction, diuretics for edema, and lipid management. Evaluate and treat secondary causes (drugs, infections, autoimmune disease, malignancy). Reserve immunosuppression for persistent nephrotic-range proteinuria or declining renal function—options include rituximab, cyclophosphamide with steroids, or calcineurin inhibitors. Monitor kidney function, proteinuria, and PLA2R antibodies.