Has your management of post-transplant FSGS changed with the advent of new FSGS directed therapies?
The pathogenesis of FSGS and specifically recurrent FSGS post-transplant has remained an unmet need in nephrology. Multiple purported " circulating permeability factors " have been identified over the years, each of them providing a piece of the picture, but none that comprehensively and definitively explain the mechanism by which podocyte injury occurs. From suPAR, cardiotropin-like cytokine gfactor1, ANGL-4, sCD40L, TNF alpha, to anti-nephrin antibodies, the list goes on. There is still much work that needs to be done in identifying the appropriate biomarkers, both for diagnosis and for monitoring response to treatment, and the specific target of pathways that are involved in the pathogenesis of FSGS. There was interest in the use of anti...
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Our protocol for recurrent FSGS is constantly evolving. We are still doing 9 runs of plasmapheresis for early recurrence (within 6 months), sometimes. using Daratumab. Later recurrence is typically treated with ACEi/ARB, with consideration for daratumamab. We have not yet routinely used the newer agents that blod ET-1 and AngII
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