BACKGROUND: 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. METHODS: 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. 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.
BACKGROUND: 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. METHODS: 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. 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.
Authors: A Sharif; M Hecking; A P J de Vries; E Porrini; M Hornum; S Rasoul-Rockenschaub; G Berlakovich; M Krebs; A Kautzky-Willer; G Schernthaner; P Marchetti; G Pacini; A Ojo; S Takahara; J L Larsen; K Budde; K Eller; J Pascual; A Jardine; S J L Bakker; T G Valderhaug; T G Jenssen; S Cohney; M D Säemann Journal: Am J Transplant Date: 2014-08-06 Impact factor: 8.086
Authors: Jana Ekberg; Henrik Ekberg; Bente Jespersen; Ragnar Källen; Karin Skov; Michael Olausson; Lars Mjörnstedt; Per Lindnér Journal: Transplant Res Date: 2014-06-13