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N Engl J Med. 2013 Dec 19;369(25):2416-23. doi: 10.1056/NEJMoa1304572. Epub 2013 Nov 8.

Abatacept in B7-1-positive proteinuric kidney disease.

Author information

1
From the Department of Medicine, Massachusetts General Hospital and Harvard Medical School (C.-C.Y., A.W., S.H., D.B., M.A.A., A.G., P.M.), Department of Pathology, Brigham and Women's Hospital and Harvard Medical School (A.W.), and Division of Nephrology, Children's Hospital Boston (P.F.) - all in Boston; the Graduate Institute of Medicine, College of Medicine (C.-C.Y.), and Department of Internal Medicine (J.-M.C., H.-C.C.), Kaohsiung Medical University, Kaohsiung, Taiwan; the Division of Nephrology and Hypertension (A.F., D.M., M.H.F., C.F., V.G.) and Lilian Jean Kaplan Division of Kidney-Pancreas Transplantation, Miami Transplant Institute, Department of Surgery (J.S., L.C., G.C., G.W.B.), University of Miami Miller School of Medicine, Miami; the Division of Nephrology, Mount Sinai School of Medicine, New York (K.N.C.); and Pediatric Nephrology, Children's Hospital, University Medical Center Hamburg-Eppendorf, Hamburg, Germany (J.O.).

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.

PMID:
24206430
PMCID:
PMC3951406
DOI:
10.1056/NEJMoa1304572
[Indexed for MEDLINE]
Free PMC Article

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