Abstract
Drug-induced kidney injury accounts for 20% of community- and hospital-acquired cases of acute kidney injury (AKI). The incidence is higher among older individuals, who often have co-existing morbidities and are exposed to more diagnostic procedures and therapies. While demographic and clinical components have been identified as risk factors, the proposed cellular mechanisms of drug-induced kidney injury are numerous and complicated. There are also limitations recognized in the use of traditional biomarkers, such as serum creatinine and blood urea nitrogen, to provide high sensitivity, specificity, and timeliness to identification of drug-induced kidney injury. Therefore, novel biomarkers are currently being investigated, identified, developed, and validated for their performance over the traditional biomarkers. This review will provide an overview of drug-induced kidney injury and will discuss what is known regarding "omic" (proteomic, genomic, transcriptomic, and metabolomic) biomarker strategies for drugs known to induce nephrotoxicity.