Published in
Lippincott, Williams & Wilkins, Pharmacogenetics and Genomics, 5(22), p. 373-380, 2012
DOI: 10.1097/fpc.0b013e328351f3c1
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The new CYP3A4 intron 6 C>T polymorphism (CYP3A4*22) is associated with an increased risk of delayed graft function and worse renal function in cyclosporine-treated kidney transplant patients.
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Rachida Bouamar,
Dennis A. Hesselink,
Vincent Haufroid,
Teun van Gelder,
Ron H. N. van Schaik
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Abstract
Cyclosporine A (CsA) is a substrate of cytochrome P450 3A4 (CYP3A4). Recently, a newly discovered intron 6 single-nucleotide polymorphism in CYP3A4 (rs35599367 C>T), defining the CYP3A4*22 allele, has been linked to reduced hepatic expression and activity of CYP3A4. In the present study, the clinical impact of this single-nucleotide polymorphism was investigated in a cohort of patients receiving a CsA-based immunosuppressive regimen.