Acute kidney injury in patients with inactive cytochrome P450 polymorphisms

Nelson Leung, Alfonso Eirin, Maria V. Irazabal, Daniel E. Maddox, Heidi D. Gunderson, Fernando C. Fervenza, Vesna D. Garovic

Research output: Contribution to journalArticlepeer-review

3 Scopus citations


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 languageEnglish (US)
Pages (from-to)749-752
Number of pages4
JournalRenal Failure
Issue number8
StatePublished - 2009


  • Acute kidney injury
  • Cytochrome P450
  • Interstitial nephritis

ASJC Scopus subject areas

  • Critical Care and Intensive Care Medicine
  • Nephrology


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