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Table 1 List of drugs/drug classes associated with pseudo-AKI and their possible mechanism(s)

From: Moving toward a contemporary classification of drug-induced kidney disease

Drugs/drug classes

Mechanism(s)

Antibiotics/antivirals:

Trimethoprim, pyrimethamine, cobicistat, dolutegravir

Antiarrhythmics:

Dronedarone

Gastrointestinal agents:

Cimetidine

Antineoplastics:

Tyrosine kinase inhibitors (e.g., imatinib, bosutinib, sorafenib, sunitinib, crizotinib, gefitinib, and pazopanib)

Poly-ADP-ribose polymerase inhibitors (e.g., olaparib, niraparib talazoparib)

Cyclin-dependent kinase 4/6 inhibitors (e.g., palbociclib, abemaciclib, ribociclib)

Anaplastic lymphoma kinase inhibitors (e.g., crizotinib, ceritinib, alectinib, brigatinib, lorlatinib)

Others:

Probenecid

Competing with and decreasing proximal tubule creatinine secretion in a dose-dependent manner, mediated via the inhibition of drug efflux transporters such as organic cation transporter

Creatine supplements

(both short term and long term)

Increasing the precursor of creatinine

Corticosteroids

Increasing catabolic state is associated with the release of creatine from muscle, spontaneously converted to creatinine

Some formulations of dexamethasone may contain creatinine as a buffer excipient.

Azasetron

Some formulations may contain creatinine as a buffer excipient.

Fenofibrate

Increasing the metabolic production of creatinine

Cephalosporins (e.g., cephalothin, cefazolin, cephalexin, cefoxitin, cefaclor, cephradine), clavulanic acid

Interfering with the analytical measurement of creatinine (Jaffe method)

5-Flucytosine

Interfering with the analytical measurement of creatinine (Ektachem enzymatic system)

Calcitriol and alfacalcidol

Unknown

  1. Pseudo-AKI via inhibiting organic anion transporters 1 & 3 in proximal tubule has also been reported with antibiotic combinations such as piperacillin/tazobactam or vancomycin plus piperacillin/tazobactam [17, 18]. Nevertheless, interstitial nephritis due to piperacillin/tazobactam has been documented in the literature [19, 20]. Thus, it seems prudent not to place piperacillin/tazobactam into the “neither dysfunction nor damage” category
  2. Sulfamethoxazole/trimethoprim should be discriminated from trimethoprim alone and viewed as an independent agent because of described interstitial nephritis or crystal nephropathy cases induced by sulfamethoxazole/trimethoprim [21]. Therefore, sulfamethoxazole/trimethoprim may not match the “neither dysfunction nor damage” category