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B7-1 Blockade Does Not Improve Post-Transplant Nephrotic Syndrome Caused by Recurrent FSGS.

Authors
  • Delville, Marianne
  • Baye, Emilie
  • Durrbach, Antoine
  • Audard, Vincent
  • Kofman, Tomek
  • Braun, Laura
  • Olagne, Jérôme
  • Nguyen, Clément
  • Deschênes, Georges
  • Moulin, Bruno
  • Delahousse, Michel
  • Kesler-Roussey, Gwenaëlle
  • Beaudreuil, Séverine
  • Martinez, Frank
  • Rabant, Marion
  • Grimbert, Philippe
  • Gallazzini, Morgan
  • Fabiola Terzi
  • Legendre, Christophe
  • Canaud, Guillaume
Type
Published Article
Journal
Journal of the American Society of Nephrology
Publisher
American Society of Nephrology (ASN)
Publication Date
Dec 29, 2015
Volume
27
Issue
8
Pages
2520–2527
Identifiers
DOI: 10.1681/ASN.2015091002
PMID: 26701979
PMCID: PMC4978058
Source
USPC - SET - SVS
Keywords
License
Green

Abstract

FSGS 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.

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