• Journal of critical care · Dec 2015

    Observational Study

    Whole-blood neutrophil gelatinase-associated lipocalin to predict adverse events in acute kidney injury: A prospective observational cohort study.

    • Oleksa Rewa, Ron Wald, Neill K J Adhikari, Michelle Hladunewich, Stephen Lapinsky, John Muscedere, Sean M Bagshaw, Orla M Smith, Gerald Lebovic, Rottem Kuint, and David J Klein.
    • Interdepartmental Division of Critical Care Medicine, University of Toronto, 2075 Bayview Ave, Room D1.08, Toronto, ON, Canada M4N 3M5. Electronic address: oleksa.rewa@utoronto.ca.
    • J Crit Care. 2015 Dec 1; 30 (6): 1359-64.

    PurposeAcute kidney injury is common in intensive care units and is associated with increased morbidity and mortality. We evaluated the ability of whole-blood neutrophil gelatinase-associated lipocalin (wbNGAL) to predict mortality and need for renal replacement therapy (RRT) in critically ill patients with kidney dysfunction.MethodsWe prospectively enrolled adult patients in 5 Canadian intensive care units. We measured wbNGAL at the time of enrollment to determine whether NGAL concentration could predict the primary composite outcome of death or need for RRT by day 30 in addition to other secondary outcomes.ResultsWe recruited 234 patients; 227 were included in the analysis. In a multivariable model, wbNGAL did not predict 30-day mortality or need for RRT (odds ratio, 1.05; 95% confidence interval, 0.99-1.12). Neutrophil gelatinase-associated lipocalin was similar in patients who died (654 [303-1180] ng/mL) vs those who survived (541.5 [255.5-1080] ng/mL, P=.26) by 90 days. Whole-blood NGAL poorly predicted the primary outcome (area under receiver operator curve, 0.65; 95% confidence interval, 0.58-0.73).ConclusionsIn a cohort of critically ill patients with abnormal kidney function, wbNGAL was not effective in the prediction of death or RRT within 30 days. These data do not support the use of this biomarker for the detection of clinical outcomes in this population.Crown Copyright © 2015. Published by Elsevier Inc. All rights reserved.

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