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Review
. 2020 Dec 2:13:687-705.
doi: 10.2147/PGPM.S239471. eCollection 2020.

Identification of Novel Biomarkers for Predicting Kidney Injury Due to Drugs Using "Omic" Strategies

Linda Awdishu  1 , Amandla Atilano-Roque  2 , Stacey Tuey  2 , Melanie S Joy  2   3
Affiliations
Review

Identification of Novel Biomarkers for Predicting Kidney Injury Due to Drugs Using "Omic" Strategies

Linda Awdishu et al. Pharmgenomics Pers Med. .

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.

Keywords: drug-induced kidney injury; genomics; metabolomics; proteomics; transcriptomics.

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Conflict of interest statement

The authors report no conflicts of interest for this work.

Figures

Figure 1
Figure 1
Figure depicts factors contributing to the development of kidney injury. Susceptibility of the kidney to toxic injury has been identified in polymorphisms of gap junction proteins and detoxification enzymes. Polymorphisms in drug metabolism or transport can lead to increased exposure of nephrotoxicants. Immune-mediated adverse effects from drugs may be related to genetic polymorphisms in human leukocyte antigens. Lastly, cellular repair mechanisms may be altered increasing the risk of apoptosis and tubular injury from nephrotoxicants.
See this image and copyright information in PMC

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