Table 4

Drugs with renally eliminated active or toxic metabolites that may accumulate in AKI

Drug

Drug class

Accumulated substance

Clinical consequence of metabolite accumulation


Allopurinol

Xanthine oxidase inhibitor

Active metabolite oxypurinol

Increased risk for immune-mediated hypersensitivity reaction

Codeine

Opioid analgesic

Active metabolites norcodeine and morphine

CNS depression, respiratory depression

Dolasetron

Antiemetic

Active metabolite hydrodolasetron

Q-T prolongation/ECG changes

Meperidine

Opioid analgesic

Toxic metabolite normeperidine

Anxiety, agitation, tremors, twitches, myoclonus, seizure

Midazolam

Benzodiazepine

Active metabolites 1-hydroxymidazolam and 1-hydroxymidazolamglucuronide

Apnea, sedation, drowsiness

Morphine

Opioid analgesic

Active metabolite morphine-6-glucuronide

CNS depression, respiratory depression

Mycophenolate mofetil/mycophenolic acid

Immunosuppressant

Inactive glucuronide metabolite displacing mycophenolic acid from albumin and resulting in increased free mycophenolic acid concentration

Leukopenia

Procainamide

Anti-arrhythmic

Active metabolite N-acetyl procainamide (NAPA)

Sinus bradycardia, sinus node arrest, Q-T interval prolongation

Propoxyphene

Opioid analgesic

Active metabolite norpropoxyphene

Cardiotoxicity resulting in dysrhythmias

Quinidine

Anti-arrhythmic, antimalarial

Active metabolite 3-hydroxy quinidine

Additive Q-T interval prolongation

Voriconazole – intravenous formulation

Antifungal

Vehicle sulfobutyl ether β-cyclodextran sodium (SBECD)

Demonstrated proximal tubule toxicity in rats


Data from [37,39,40,43,76-82]. AKI, acute kidney injury.

Vilay et al. Critical Care 2008 12:235   doi:10.1186/cc7093