| Title | Acute kidney injury in patients with inactive cytochrome p450 polymorphisms. | | Author(s) | Leung N, Eirin A, Irazabal MV, Maddox DE, Gunderson HD, Fervenza FC, Garovic VD | | Institution | Mayo Clinic Rochester, Division of Nephrology and Hypertension, Rochester, Minnesota, USA. | | Source | Ren Fail 2009; 31(8):749-52. | | Abstract | Medications are a major source of acute kidney injury, especially in critically ill patients. Medication-induced renal injury can occur through a number of mechanisms. We present two cases of acute kidney injury (AKI) where inactive cytochrome P450 (CYP) polymorphism may have played a role. The first patient developed a biopsy-proven allergic interstitial nephritis following urethrotomy. Genetic testing revealed the patient to be heterozygous for an inactivating polymorphism CYP2C9*3 and homozygous for an inactivating polymorphism CYP2D6*4. Patient had received several doses of promethazine, which is metabolized by CYP2D6*4. Another patient developed AKI on several occasions after exposure to lansoprazole and allopurinol. CYP testing revealed the patient to be homozygous for inactivating polymorphism CYP2C19*2, which is responsible for the metabolism of lansoprazole. These are the first two cases of AKI associated with non-functional polymorphisms of cytochrome P450 superfamily. While the exact mechanism has not been worked out, it introduced the possibility of a new source of kidney injury. | | Language | eng | | Pub Type(s) | Journal Article
| | PubMed ID | 19814645 |
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