Published in
Lippincott, Williams & Wilkins, Pharmacogenetics and Genomics, 12(23), p. 649-657, 2013
DOI: 10.1097/fpc.0000000000000001
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Single-nucleotide polymorphisms in P450 oxidoreductase and peroxisome proliferator-activated receptor-α are associated with the development of new-onset diabetes after transplantation in kidney transplant recipients treated with tacrolimus.
,
Ferdi Sombogaard,
Dennis A. Hesselink,
Ron H. N. van Schaik,
Teun van Gelder
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Abstract
New-onset diabetes after transplantation (NODAT) is an important complication after kidney transplantation. The etiology of the malady is multifactorial and includes both environmental and genetic factors. NODAT is a polygenic disease and many single-nucleotide polymorphisms could constitute potential risk factors. Peroxisome proliferator-activated receptor α (PPARα) and P450 oxidoreductase (POR) play a central role in the control of energy metabolism in humans. Some recent data highlighted a possible functional impact of two single-nucleotide polymorphisms in PPARα (rs4253728 G>A and rs4823613 A>G) and one coding variant in POR (rs1057868; POR*28; A503V) on the activity of their respective encoded proteins. In the present study, we assessed the association between these variants and the risk of developing NODAT after kidney transplantation.