Abatacept in B7-1–Positive Proteinuric Kidney Disease

Chih Chuan Yu(Harvard University), Alessia Fornoni(University of Miami), Astrid Weins(Brigham and Women's Hospital), Samy Hakroush(Harvard University), Dony Maiguel(University of Miami), Junichiro Sageshima(University of Miami), Linda Chen(University of Miami), Gaetano Ciancio(University of Miami), Mohd Hafeez Faridi(University of Miami), Daniel S. Behr(Harvard University), Kirk N. Campbell(Icahn School of Medicine at Mount Sinai), Jer Ming Chang(Kaohsiung Medical University), Hung Chun Chen(Kaohsiung Medical University), Jun Oh(Universität Hamburg), Christian Faul(University of Miami), M. Amin Arnaout(Harvard University), Paolo Fiorina(Boston Children's Hospital), Vineet Gupta(University of Miami), Anna Greka(Harvard University), George W. Burke(University of Miami), Peter Mündel(Harvard University)
New England Journal of Medicine
November 8, 2013
10.1056/nejmoa1304572
Cited by 377Open Access
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Abstract

Abatacept (cytotoxic T-lymphocyte-associated antigen 4-immunoglobulin fusion protein [CTLA-4-Ig]) is a costimulatory inhibitor that targets B7-1 (CD80). The present report describes five patients who had focal segmental glomerulosclerosis (FSGS) (four with recurrent FSGS after transplantation and one with primary FSGS) and proteinuria with B7-1 immunostaining of podocytes in kidney-biopsy specimens. Abatacept induced partial or complete remissions of proteinuria in these patients, suggesting that B7-1 may be a useful biomarker for the treatment of some glomerulopathies. Our data indicate that abatacept may stabilize β1-integrin activation in podocytes and reduce proteinuria in patients with B7-1-positive glomerular disease.

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