Nephrotoxicity is frequently seen with many commonly used medications today. This is not surprising given the consideration of renal vascular beds receiving approximately 25% of cardiac output which causes nephrotoxin to accumulate in the kidney (1). Furthermore, the renal tubules present a substantial area for drug binding and transport via numerous enzymes and transtubular transport processes, which lead to contact with drugs or their metabolites at greater concentrations than expected. Drug-related renal injury (DRI) can present a wide range of clinical spectrum via multiple mechanisms, and some of them can cause more than one pattern of injury (Table 1). Drugs can also cause about 20% of community-and hospitalacquired episodes of acute renal injury (AKI) (2, 3). The incidence of DRI is increasing in modern society mainly due to increasing aging population who are more prone to comorbidities and the chance of exposure to diagnostic and therapeutic procedures (2-4). In fact, the true incidence of drug-induced renal diseases is diffi cult to establish since clinical presentations are quite variable with the uncertainty of causality at times. The mechanisms of DRI may differ between different drugs, and they are generally categorized based on the pathologic characteristics of the affected kidney (Table 2) (5).