Biomarkers of drug-induced acute kidney injury in the adult

Glenda C Gobe, Jeff S Coombes, Robert G Fassett, Zoltan H Endre

This article addresses general biomarkers of drug-induced acute kidney injury (AKI) and their application in development and progression of AKI in the adult. It also highlights some clinical benefits, but also uncertainties, of biomarker use. Drug-induced AKI is traditionally diagnosed by monitoring serum creatinine (SCr), blood urea nitrogen and albuminuria. The sensitivity of these measures is, however, limited to well-established AKI. Application of selected biomarkers for early diagnosis of drug-induced AKI may inform on progression of AKI and alert clinicians to adopt renoprotective strategies at the earliest times. Novel biomarkers, accepted for early detection of drug-induced AKI (kidney injury molecule-1, neutrophil gelatinase-associated lipocalin and N-acetyl-β-d-glucosaminidase), may be useful additions in panels of biomarkers. Clinical biomarkers of cell cycle arrest, tissue inhibitor of metalloproteinase-2 and insulin-like growth factor binding protein 7 show promise but need further validation in clinical trials. Traditional parameters, such as SCr, provide some guidance for functional decline in drug-induced AKI but early, more sensitive, affordable, clinically acceptable, biomarkers of kidney dysfunction are needed. Basic biological understanding of AKI will improve with high-throughput methodologies such as proteomics and metabolomics, and this should lead to identification and usage of novel biomarkers. Ultimately, a combination of biomarkers indicating kidney dysfunction and damage is likely to be required.