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NDT Advance Access published online on November 23, 2009
Nephrology Dialysis Transplantation, doi:10.1093/ndt/gfp617
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© The Author 2009. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org


Impaired glucose homeostasis in renal transplant recipients receiving basiliximab

Willy Aasebø1, Karsten Midtvedt1, Tone Gretland Valderhaug2, Torbjørn Leivestad3, Anders Hartmann1,4, Anna Varberg Reisæter1, Trond Jenssen1,5 and Hallvard Holdaas1

1 Section of Nephrology, Rikshospitalet University Hospital, Oslo University Hospital, 0027 Oslo, Norway 2 Thoracic surgical department, Rikshospitalet University Hospital, Oslo University Hospital, 0027 Oslo Norway 3 Institute of Immunology, Rikshospitalet University Hospital, Oslo, Norway 4 Faculty of Medicine, University of Oslo, Oslo, Norway 5 Institute of Clinical Medicine, University of Tromso, NO-9037 Tromso, Norway

Correspondence and offprint requests to: Willy Aasebø; E-mail: willy.aaseboe{at}rikshospitalet.no, waaseboe{at}online.no



  Abstract

Background. The pathogenesis of new onset diabetes after transplantation (NODAT) is multifactorial. Suppression of regulatory T lymphocytes may have a negative impact on pancreatic β-cells. Induction with basiliximab affects regulatory T-cell function and may therefore, theoretically, also affect glucose homeostasis in renal transplant recipients.

Methods. All kidney recipients ≥50 years of age without diabetes mellitus transplanted from 1 January 2005 to 31 December 2007 were included in a single-centre retrospective study. Immunosuppression consisted of steroids, mycophenolate mofetil and cyclosporine. Basiliximab was introduced as induction therapy 1 January 2007. An oral glucose tolerance test (OGTT) was performed in all patients 10 weeks post-transplant.

Results. A total of 264 patients were recruited. One hundred and thirty-four patients received basiliximab. In the basiliximab group, 51.5% developed NODAT, impaired glucose tolerance (IGT) or impaired fasting glucose (IFG) versus 36.9% in the group without induction therapy (P = 0.017). In recipients with normal OGTT, the mean fasting glucose at 10 weeks was 5.18 mmol/l (SD: 0.54) in the basiliximab group (n = 65) and 4.84 mmol/l (SD: 0.64) in the no induction group (n = 82) (P = 0.001).

Conclusion. Use of basiliximab as induction therapy may be associated with impaired glucose homeostasis after kidney transplantation.

Keywords: diabetes mellitus; immunosuppression; kidney transplantation; pathogenesis

Received for publication: 18. 5.09
Accepted in revised form: 23.10.09


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