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Am J Physiol Renal Physiol. 2016 Oct 1;311(4):F717-F721. doi: 10.1152/ajprenal.00268.2016. Epub 2016 Jul 27.

Bench to bedside: the next steps for biomarkers in acute kidney injury.

Author information

1
Department of Medicine, University of Otago Christchurch, Christchurch, New Zealand; Emergency Department, Christchurch Hospital, Christchurch, New Zealand; John.Pickering@otago.ac.nz.
2
Department of Nephrology, Prince of Wales Hospital, Sydney, Australia; and Prince of Wales Clinical School, University of New South Wales, Sydney, Australia.

Abstract

No new biomarker of acute kidney injury (AKI) has entered routine clinical practice after a decade of promise, although liver-fatty acid binding protein (L-FABP), neutrophil gelatinase-associated lipoprotein (NGAL), and the combination of tissue inhibitor of metalloproteinase 2 (TIMP-2) and insulin-like growth factor-binding protein 7 (IGFBP-7) are approved for use in some jurisdictions. Acceptance of creatinine as a surrogate of not just glomerular filtration rate (GFR) but also renal injury, changes in nephrologist workloads, failure to establish the added value of each biomarker to current clinical variables across multiple clinical settings, the lack of treatment options, and simply an insufficient passage of time, have all contributed to the lack of progress. Future studies should establish reference intervals for biomarkers, associate biomarkers with meaningful clinical outcomes including mortality and development of chronic kidney disease, and assess the added value to clinical models. The real value of biomarkers will be determined with intervention trials that use an elevated biomarker to triage to treatment. Ideally, such treatments will be linked directly to the physiological processes, which the biomarker identifies.

KEYWORDS:

acute kidney injury; acute renal failure; biomarkers; translational

PMID:
27465990
DOI:
10.1152/ajprenal.00268.2016
[Indexed for MEDLINE]
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