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. Author manuscript; available in PMC: 2016 Feb 18.
Published in final edited form as: Kidney Int. 2015 Apr 8;88(2):226–234. doi: 10.1038/ki.2015.115

Table 2. Drug toxicity mechanism and timing for AKI and Glomerular phenotypes.

Drug AKI Glomerular Time Course Genetic Mechanism
Type A Type B Type A Type B
Abacavir X Acute HLA
Aminoglycosides X Acute/SA Megalin/Cathepsins/Caspases
Amoxicillin X SA HLA
Ampicillin X SA HLA
Amphotericin X Acute/SA
Bevacizumab X SA VEGF
Cefazolin X SA HLA
Ceftazidime X SA HLA
Cidofovir X Acute OAT
Ciprofloxacin X SA HLA
Colistin X SA OCT
Cyclosporine X X Acute/SA CYP 3A/PGP
Foscarnet X Acute/SA
Hydralazine X SA/Chronic HLA
Levofloxacin X SA HLA
Lithium X SA/Chronic VA receptors
Nafcillin X SA HLA
NSAIDs X X Acute/SA HLA
Oxacillin X SA HLA
Pamidronate X X SA
Penicillin X SA HLA
Piperacillin/tazobactam X Acute/SA HLA
Propylthiouracil X SA/Chronic HLA
Rifampin X X SA HLA
SMX/TMP X Acute/SA HLA
Tacrolimus X X Acute/SA CYP 3A
Vancomycin X X Acute/SA Oxidative stress, HLA

Type A= dose dependent toxicity, Type B= idiosyncratic, acute = within 7 days of drug initiation, SA = sub-acute, occurs within 4 weeks of drug exposure and may take up to 90 days to resolve, chronic = injury persisting beyond 90 days, OAT=organic anion transporter, HLA = human leukocyte antigen, CYP = cytochrome P450, PGP = p-glycoprotein, MRP = multi-drug resistance associated protein