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.
Original language | English (US) |
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Pages (from-to) | 749-752 |
Number of pages | 4 |
Journal | Renal Failure |
Volume | 31 |
Issue number | 8 |
DOIs | |
State | Published - 2009 |
Keywords
- Acute kidney injury
- Cytochrome P450
- Interstitial nephritis
ASJC Scopus subject areas
- Critical Care and Intensive Care Medicine
- Nephrology