Impaired glucose homeostasis in renal transplant recipients receiving basiliximab

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

All kidney recipients > or =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.

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).

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