In recent years, rituximab has been gradually used in the treatment of idiopathic membranous nephropathy (IMN). Compared with traditional treatments, the safety and effectiveness of rituximab in the treatment of IMN have been confirmed, which induces remission in 60%-80% of patients. For the remaining 20%-40% patients, several mechanisms can explain rituximab resistance: decreased rituximab bioavailability; internalized by targeted B cells; the generation of anti-rituximab antibody; chronic and irreversible damage to the glomerular filtration barrier; autoreactive B-cell clones in secondary lymphoid organs that cannot be effectively eliminated. The treatment of patients with rituximab-refractory IMN remains controversial and challenging. The recognition of IMN as an antibody-mediated autoimmune disease has rationalized the use of immunosuppressive drugs such as B cell-targeted therapies, plasma cell-targeted therapies, and complement inhibitors. This review mainly summarizes recent advances in the understanding of the physiological mechanisms of rituximab resistance, and in the management of rituximab-refractory IMN, aiming to aid in the clinical management of IMN.