Cresents in membranous nephropathy
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Crescents in Membranous Nephropathy: Insights and Advances
Introduction to Membranous Nephropathy
Membranous nephropathy (MN) is a significant cause of nephrotic syndrome in adults, characterized by the deposition of immune complexes along the subepithelial region of the glomerular basement membrane. This condition can lead to severe kidney damage and is a leading cause of end-stage renal disease in patients with primary glomerulonephritis.
Pathogenesis and Key Antigens
Immune Complex Deposition
The pathogenesis of MN involves the formation of immune deposits on the outer aspect of the glomerular basement membrane. These deposits contain podocyte or planted antigens and circulating antibodies specific to those antigens, resulting in complement activation.
Identified Antigens
Two major antigens, phospholipase A2 receptor (PLA2R) and thrombospondin type-1 domain-containing 7A (THSD7A), have been identified as targets for these immune complexes, accounting for approximately 60% of all MN cases . The identification of these antigens has significantly advanced the understanding and diagnosis of MN. Measurement of anti-PLA2R antibodies in serum and detection of PLA2R antigen in glomerular deposits are now routine practices, aiding in the diagnosis and monitoring of treatment.
Novel Antigens
Recent advances using laser microdissection and mass spectrometry have identified additional antigens associated with MN, including exotosin 1 (EXT1), exotosin 2 (EXT2), NELL1, Sema3B, and PCDH7. Each of these represents a distinct disease entity with unique clinical and pathological findings. This highlights the importance of mass spectrometry in the accurate diagnosis and classification of MN based on detected antigens.
Treatment Approaches
Rituximab vs. Cyclosporine
Treatment of MN often involves immunosuppressive therapies. A study comparing rituximab and cyclosporine found that rituximab was noninferior to cyclosporine in inducing complete or partial remission of proteinuria at 12 months and superior in maintaining remission up to 24 months. Specifically, 60% of patients in the rituximab group achieved remission at 24 months compared to 20% in the cyclosporine group. Additionally, rituximab led to a faster and more sustained decline in anti-PLA2R antibodies among patients in remission.
Safety and Efficacy
The study also reported fewer serious adverse events in the rituximab group (17%) compared to the cyclosporine group (31%), suggesting a better safety profile for rituximab. These findings support the use of rituximab as a more effective and safer option for long-term management of MN.
Conclusion
The understanding of membranous nephropathy has significantly advanced with the identification of key antigens and the development of targeted therapies. The use of rituximab shows promise in achieving and maintaining remission with a favorable safety profile. Continued research into novel antigens and treatment responses will further enhance the management and outcomes for patients with MN.
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