Abstract: Membranous nephropathy (MN) is characterized by subepithelial immune complex deposition in the glomerular basement membrane and diffuse thickening of the basement membrane. Approximately 70% to 80% of these patients are termed idiopathic membranous nephropathy (IMN) due to the poorly defined pathogenesis. In recent years, the pathogenic role of B lymphocytes in MN has gained attention, as autoantibodies such as anti-phospholipase A2 receptor (PLA2R) antibodies and thrombospondin type-1 domain-containing 7A (THSD7A) have been identified in the peripheral blood of IMN patients. Rituximab (RTX), a human/mouse chimeric monoclonal antibody, can deplete CD20⁺ B lymphocytes by reducing the production of autoantibodies. B lymphocytes and T lymphocytes complement each other in function. Studies have confirmed that IMN patients also have disorders in the number and function of T lymphocyte subpopulations. Therefore, RTX correction of T lymphocyte subpopulations imbalance may be another important mechanism for its effect. This article reviewed the impact of rituximab treatment on peripheral blood T lymphocytes in patients with IMN and its clinical significance, providing a theoretical basis for multi-target treatment of IMN.