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By Sharma S Prabhakar

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Asanuma K et al 2003, Tryggvason K. et al. 2006). Mutations in podocin (a transmembrane protein that interacts with nephrin, NEPH-1 and CD2AP) have been identified in familial FSGS. Recently, mutations in CD2AP, an immunoglobulin-like protein that is involved in nephrin integration with podocyte cytoskeleton, have also been linked to genetic forms of FSGS (Shih NY. et al. 1999, Kim JM et al 2003, Tyggvason K. et al 2006). In mouse models, the loss of FAT1 and FAT2 (transmembrane proteins with cadherin-like repeats) results in the absence of slit diaphragms, proteinuria, and early death.

It could use the anti- PLA2R as an initial assay for the diagnosis of idiopathic MN without kidney biopsy. Serial assays for the presence and titer of anti-PLA2R prior to therapeutic intervention in clinical trials could help reduce uncertainty as to whether rapid responders represent a true therapeutic effect or a spontaneous remission. Anti-PLA2R could also be followed during treatment to assess the efficacy of immunosuppressive therapy and to determine the length of treatment. It could also be useful in partial remission, when residual proteinuria could be caused either by ongoing but attenuated immune activity or by structural glomerular changes without immune activity.

Membranous nephropathy:recent travels and new roads ahead Kidney International (2010) 77, 765–770 Beck L. Membranous Nephropathy and Malignancy,Seminars in Nephrology, Vol 30, No 6, November 2010, pp 635-644 Bomback A , Derebail V, McGregor JG, Kshirsagar AJ, FalkRJ ,PatrickH. Rituximab Therapy for Membranous Nephropathy:A Systematic Review Clin J Am Soc Nephrol 4: 734–744, 2009. 05231008 BrantenA, du Buf-Vereijken PW. Clin J Am Soc Nephrol 2: 932-937, 2007 Cattran D, Management of Membranous Nephropathy: When and What for Treatment: J Am Soc Nephrol 16: 1188–1194,2005 Cattran DC .

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