Anti-glomerular basement membrane (GBM) nephritis is a rare, life-threatening autoimmune disease characterized by rapidly progressive glomerulonephritis (RPGN) with or without diffuse alveolar hemorrhage (DAH). The disease mechanism involves intrinsic anti-GBM antibodies attacking autoantigens expressed on the basement membranes of glomerulus, resulting in crescent formation.1 The standard treatment regimen for anti-GBM nephritis comprises plasmapheresis, along with corticosteroids and cyclophosphamide (CTX).2 Therapeutic plasma exchange (TPE) is a pivotal method for the rapid elimination of autoimmune antibodies and immune complexes (ICs) from the circulation. Several large cohort studies enrolling Chinese, American, and Japanese patients have shown that TPE markedly improved the prognoses of patients with anti-GBM nephritis.3, 4, 5

However, TPE has notable drawbacks because it indiscriminately removes beneficial plasma components and consumes a large volume of plasma or albumin (ALB).6 Double-filtration plasmapheresis (DFPP) has emerged as an alternative strategy for managing anti-GBM nephritis. As a semi-selective modality of plasmapheresis, DFPP uses an additional membrane to selectively filter high-molecular-weight plasma components, sparing low-molecular-weight constituents such as ALB and coagulation factors. In recent decades, DFPP has gained acceptance in regions with scarce plasma supplies, being applied in the treatment of multisystem disorders, such as myasthenia gravis, systemic lupus erythematosus, familial hypercholesterolemia, and thrombotic thrombocytopenic purpura.7 However, there is limited research on the application of DFPP in anti-GBM nephritis,8 and the comparative safety and efficacy of TPE versus DFPP remain uncertain. Hence, we conducted a retrospective cohort study to clarify the similarities and differences between the two modalities of plasmapheresis, thereby providing evidence for the clinical application of DFPP in anti-GBM nephritis.