Nickan Research Institute Journal of Renal Injury Prevention 2345-2781 7 1 2018 03 01 Anti-phospholipase A2 receptor antibody in membranous nephropathy; an Indian experience 16 21 10.15171/jrip.2018.04 EN Monika Yachha Raj Kumar Sharma Sonia Mehrotra Narayan Prasad Amit Gupta Anupma Kaul Dharmendra Singh Bhadauria Journal Article 10.15171/jrip.2018.04 2017 04 04 2017 08 08 Introduction: Autoantibodies against phospholipase-A2 Receptor (PLA2 R), a normally occurring antigen presented on podocyte membranes, have recently been implicated in the pathology of membranous nephropathy (MN). Objectives: In this observational study, we have evaluated the correlation of patient’s disease activity against serum levels of anti-PLA2 R in patients with primary and secondary MN in a North Indian cohort. Patients and Methods: We measured serum anti-PLA2 R antibody by ELISA in 63 adult patients with MN. Out of these 63 patients, the majority (58) had primary MN (pMN) and the remaining five had secondary MN (sMN). Results: Around 55.2% had detectable anti-PLA2 R autoantibodies (63% in those with newonset pMN, 67% in patients with relapse and 3% in patients in remission). However, all patients with refractory pMN (n=4) were anti-PLA2 R negative. There was significantly higher anti-PLA2 R positivity in active stage of disease in contrast to those in remission (P<0.001). Autoantibody level was proportional to the disease activity, with a trend towards significance (P=0.052). Hypoalbuminemia and proteinuria were also significantly worse in the antiPLA2 R positive patients. All patients with sMN tested negative for anti-PLA2 R autoantibodies. Conclusion: PLA2 R is a major target antigen in Indian population with idiopathic MN. AntiPLA2 R positivity is a specific tool to detect idiopathic MN, and its levels correspond well with other disease activity markers. In addition, anti-PLA2 R antibody was negative in refractory pMN, which suggests the existence of additional autoantibodies in this subgroup, with a different target antigen. These autoantibodies may be resistant to the currently recommended immunosuppressants for the disease, thus the refractory nature of the disease.