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Is basiliximab induction, a novel risk factor for new onset diabetes after transplantation for living donor renal allograft recipients?
Author(s) -
Prasad Narayan,
Gurjer Desraj,
Bhadauria Dharmender,
Gupta Amit,
Srivastava Aneesh,
Kaul Anupama,
Jaiswal Akhilesh,
Yadav Brijesh,
Yadav Subhash,
Sharma Raj K
Publication year - 2014
Publication title -
nephrology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 61
eISSN - 1440-1797
pISSN - 1320-5358
DOI - 10.1111/nep.12209
Subject(s) - basiliximab , medicine , transplantation , gastroenterology , diabetes mellitus , impaired fasting glucose , impaired glucose tolerance , kidney transplantation , endocrinology , insulin resistance , insulin
Aim It was found that, by affecting populations of T lymphocytes and regulatory T cells, basiliximab also indirectly affects pancreatic β‐cell function and glucose homeostasis. Methods In this prospective observational study, we included all renal transplant recipients from 1 J uly 2007 to 31 J uly 2011. The overall incidence of hyperglycaemia (transient hyperglycaemia, impaired fasting glucose ( IFG ), impaired glucose tolerance ( IGT ) and new onset diabetes after transplantation ( NODAT )) was compared between patients with and without basiliximab induction. Results Of the 439 eligible study patients, 105 patients received basiliximab induction and 334 patients did not. Overall hyperglycaemia (transient hyperglycaemia, IFG , IGT and NODAT ) was detected in 102/334 (30.5%) patients without induction and 44/105 (41.9%) patients with induction ( P  = 0.03). Of the 102 patients with hyperglycaemia in patients without basiliximab, 46 (45.1%) patients improved, while only 10 (22.7%) of the 44 patients with basiliximab improved ( P  = 0.016) at the end of 3 months. Finally, NODAT was observed in 56/334 (16.7%) patients without induction and 102/334 (30.5%) patients with induction. Relative risk of NODAT with basiliximab was 2.3 (95% CI 1.4‐3.9) compared to that of patients without induction. Basiliximab and hepatitis C virus infection were independent risk factors for NODAT . Risk of NODAT remained high with basiliximab despite adjusting the acute rejections episodes. Conclusions Basiliximab induction prevents acute rejection; however, it is associated with increased risk of NODAT .

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