Rituximab might be working in a non B cell mediated manner in FSGS recurrence post transplant.
A new study by Fornoni et al showed this in an elegant way.
Some summary points
1. 41 patients were studied, post transplant and 14 were controls and remaining received rituxian as part of their induction.
2. Fewer podocytes with SMPDL-3b protein in biopsies from recurrent FSGS were found.
3. Serum from patients with recurrent FSGS had a decrease in both SMPDL -3b and sphingomyelinase activity.
4 They predicated that rituximab preserves SMPDL-3b expression in podocytes.
5.The above part was prevented with anti CD20 treatment.
6. They studied SMPDL-3b protein, cytoskeleton remodeling in cultured normal human podocytes that had been exposed to patient sera with or without rituximab.
7. Over-expression of SMPDL-3b or treatment with Anti CD20 was able to prevent recurrent FSGS and showed preservation of cytoskeleton.
8.These data suggest that modulation of the sphigolipid related proteins might be playing a role in causing recurrent FSGS and perhaps anti CD20 agents are inhibiting this process in a B cell independent fashion.
Key: SMPDL= sphingomyelin phosphdiesterase acid like.
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