Biomarkers of drug-induced acute kidney injury in the adult.

INTRODUCTION

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.

AREAS COVERED

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.

EXPERT OPINION

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.