Abstract Background: Membranous nephropathy (MN) is caused by autoantibody binding to podocyte foot process antigens such as THSD7A and PLA2R1. The mechanisms of the glomerular antigen/autoantibody deposition and clearance are unknown. Methods: We explore the origin and significance of glomerular accumulations in (1) diagnostic and follow-up biospecimens from THSD7A+ and PLA2R1+-MN patients compared to nephrotic non-MN patients, and (2) in experimental models of THSD7A+-MN.