• Marianne Delville, Emilie Baye, Antoine Durrbach, Vincent Audard, Tomek Kofman, Laura Braun, Jérôme Olagne, Clément Nguyen, Georges Deschênes, Bruno Moulin, Michel Delahousse, Gwenaëlle Kesler-Roussey, Séverine Beaudreuil, Frank Martinez, Marion Rabant, Philippe Grimbert, Morgan Gallazzini, Fabiola Terzi, Christophe Legendre, and Guillaume Canaud.
• Université Paris Descartes, Sorbonne Paris Cité, Service de Biothérapie.
• J. Am. Soc. Nephrol. 2016 Aug 1; 27 (8): 2520-7.

AbstractFSGS is a common glomerular disorder that has a high propensity for recurrence after kidney transplant. The pathophysiology of FSGS is unknown, but podocytes seem to be the target of one or several circulating factors that lead to cytoskeleton reorganization and proteinuria. Research on podocytes has identified B7-1 as an important factor in podocyte biology and a new therapeutic target in renal disease. Indeed, in four patients with recurrent FSGS after transplant, treatment with the B7-1 blocker abatacept was associated with proteinuria remission. Here, we prospectively treated nine patients with recurrent FSGS after transplant using either abatacept or belatacept, a B7-1 blocker with higher affinity, and did not induce proteinuria remission. Furthermore, we did not detect B7-1 expression by immunofluorescence in podocytes of biopsy specimens from these or other kidney grafts or podocytes of native kidney biopsy specimens. In conclusion, B7-1 blockade did not induce FSGS remission after transplant in our study. Copyright © 2016 by the American Society of Nephrology.

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