Membranous nephropathy (MN) is a rare disease in which immune complexes deposit at the glomerular basement membrane, causing damage to the filtration barrier, resulting in proteinuria. Recent studies have shown that in approximately 70% of patients with primary MN (pMN), the immune complexes consist of autoantibodies against the podocyte protein M-type phospholipase A2 receptor (PLA2R).(1) There is also evidence that levels of anti-PLA2R autoantibodies correlate well with disease activity and progression.(2) The presence of anti-PLA2R antibodies could also potentially be used to differentiate pMN from other causes of nephrotic syndrome if a biopsy is not possible. Among patients with chronic kidney disease (CKD) awaiting kidney transplantation, higher levels of anti-PLA2R could predict those more likely to recur after transplantation.(2)

Therapy outcome can be monitored by measuring the anti-phospholipase A2 receptor (PLA2R) antibody titer. A titer increase, decrease, or disappearance generally precedes a change in clinical status. Thus, the determination of the antibody titer has a high predictive value with respect to clinical remission, relapse, or risk assessment after kidney transplantation.

Absence of circulating anti-phospholipase A2 receptor (PLA2R) autoantibodies does not rule out a diagnosis of primary MN.

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