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Table 4 Drugs with renally eliminated active or toxic metabolites that may accumulate in AKI

From: Clinical review: Drug metabolism and nonrenal clearance in acute kidney injury

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

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