Clinical use of Biomarkers for Toxicant-Induced Acute Kidney Injury

Abstract

Toxicant-induced acute kidney injury (ToxAKI) causes substantial morbidity and retards drug development. ToxAKI is relatively underexplored compared with ischemia–reperfusion injury in clinical biomarker studies. We highlight the rationale for novel AKI biomarkers in management of ToxAKI, and review the contemporary evidence supporting their clinical use. Directly-acting nephrotoxins, such as cisplatin, aminoglycosides, vancomycin and radiocontrast, remain widely used and highlight how novel biomarkers can either improve the detection of changes in glomerular filtration rate or directly signal cellular injury and structural damage. Serum cystatin C has already improved clinical risk prediction and drug dosing although its clinical use for early diagnosis awaits validation. The use of novel functional and structural biomarkers to stage ToxAKI and aid prognosis requires robust validation and better understanding of the relationship between biomarkers, morbidity and mortality. Biomarkers that illustrate the probable mechanisms and phase of ToxAKI may guide mechanism-specific diagnosis and therapy.

KEYWORDS::

• acute kidney injury
• biological markers
• cystatin C
• drug toxicity
• translational medical research

Financial & competing interests disclosure

TJ Pianta gratefully acknowledges the financial support of the Jacquot Research Entry Scholarship and a University of New South Wales Australian Postgraduate Award. ZH Endre has received research and travel support from Alere and Abbott. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.

Notes

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Additional information

Funding

TJ Pianta gratefully acknowledges the financial support of the Jacquot Research Entry Scholarship and a University of New South Wales Australian Postgraduate Award. ZH Endre has received research and travel support from Alere and Abbott. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.