Plasma endostatin may improve acute kidney injury risk prediction in critically ill patients

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Abstract

Background

Breakdown of renal endothelial, tubular and glomerular matrix collagen plays a major role in acute kidney injury (AKI) development. Such collagen breakdown releases endostatin into the circulation. The aim of this study was to compare the AKI predictive value of plasma endostatin with two previously suggested biomarkers of AKI, cystatin C and neutrophil gelatinase-associated lipocalin (NGAL).

Methods

We studied 93 patients without kidney disease who had a first plasma sample obtained within 48 h of ICU admission. We identified risk factors for AKI within the population and designed a predictive model. The individual ability and net contribution of endostatin, cystatin C and NGAL to predict AKI were evaluated by the area under the receiver operating characteristics curve (AUC), likelihood-ratio test, net reclassification improvement (NRI) and integrated discrimination improvement (IDI).

Results

In total, 21 (23 %) patients experienced AKI within 72 h. A three-parameter model (age, illness severity score and early oliguria) predicted AKI with an AUC of 0.759 (95 % CI 0.646–0.872). Adding endostatin to the predictive model significantly ( P = 0.04) improved the AUC to 0.839 (95 % CI 0.752–0.925). In addition, endostatin significantly improved risk prediction using the likelihood-ratio test ( P = 0.005), NRI analysis (0.27; P = 0.04) and IDI analysis (0.07; P = 0.04). In contrast, adding cystatin C or NGAL to the three-parameter model did not improve risk prediction in any of the four analyses.

Conclusions

In this cohort of critically ill patients, plasma endostatin improved AKI prediction based on clinical risk factors, while cystatin C and NGAL did not.

Electronic supplementary material

The online version of this article (doi:10.1186/s13613-016-0108-x) contains supplementary material, which is available to authorized users.

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Most cited references 23

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Incidence, risk factors and 90-day mortality of patients with acute kidney injury in Finnish intensive care units: the FINNAKI study.

Sara Nisula, Kirsi-Maija Kaukonen, Suvi Vaara … (2013)

We aimed to determine the incidence, risk factors and outcome of acute kidney injury (AKI) in Finnish ICUs. This prospective, observational, multi-centre study comprised adult emergency admissions and elective patients whose stay exceeded 24 h during a 5-month period in 17 Finnish ICUs. We defined AKI first by the Acute Kidney Injury Network (AKIN) criteria supplemented with a baseline creatinine and second with the Kidney Disease: Improving Global Outcomes (KDIGO) criteria. We screened the patients' AKI status and risk factors for up to 5 days. We included 2,901 patients. The incidence (95 % confidence interval) of AKI was 39.3 % (37.5-41.1 %). The incidence was 17.2 % (15.8-18.6 %) for stage 1, 8.0 % (7.0-9.0 %) for stage 2 and 14.1 % (12.8-15.4 %) for stage 3 AKI. Of the 2,901 patients 296 [10.2 % (9.1-11.3 %)] received renal replacement therapy. We received an identical classification with the new KDIGO criteria. The population-based incidence (95 % CI) of ICU-treated AKI was 746 (717-774) per million population per year (reference population: 3,671,143, i.e. 85 % of the Finnish adult population). In logistic regression, pre-ICU hypovolaemia, diuretics, colloids and chronic kidney disease were independent risk factors for AKI. Hospital mortality (95 % CI) for AKI patients was 25.6 % (23.0-28.2 %) and the 90-day mortality for AKI patients was 33.7 % (30.9-36.5 %). All AKIN stages were independently associated with 90-day mortality. The incidence of AKI in the critically ill in Finland was comparable to previous large multi-centre ICU studies. Hospital mortality (26 %) in AKI patients appeared comparable to or lower than in other studies.

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Neutrophil gelatinase-associated lipocalin in adult septic patients with and without acute kidney injury.

Johan Mårtensson, Max Bell, Anders Oldner … (2010)

To study the impact of inflammation/sepsis on the concentrations of neutrophil gelatinase-associated lipocalin (NGAL) in plasma and urine in adult intensive care unit (ICU) patients and to estimate the predictive properties of NGAL in plasma and urine for early detection of acute kidney injury (AKI) in patients with septic shock. Sixty-five patients admitted to the general ICU at the Karolinska University Hospital Solna, Sweden, with normal plasma creatinine were assessed for eligibility. Twenty-seven patients with systemic inflammatory response syndrome (SIRS), severe sepsis, or septic shock without AKI and 18 patients with septic shock and concomitant AKI were included in the final analysis. Plasma and urine were analyzed twice daily for plasma NGAL (pNGAL), C-reactive protein (CRP), procalcitonin, myeloperoxidase, plasma cystatin C, plasma creatinine, urine NGAL (uNGAL), urine cystatin C, and urine alpha1-microglobulin. Of the 45 patients, 40 had elevated peak levels of pNGAL. Peak levels of pNGAL were not significantly different between septic shock patients with and without AKI. Peak levels of uNGAL were below the upper reference limit in all but four patients without AKI. uNGAL was a good predictor (area under ROC 0.86) whereas pNGAL was a poor predictor (area under ROC 0.67) for AKI within the next 12 h in patients with septic shock. pNGAL is raised in patients with SIRS, severe sepsis, and septic shock and should be used with caution as a marker of AKI in ICU patients with septic shock. uNGAL is more useful in predicting AKI as the levels are not elevated in septic patients without AKI.

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The Rise and Fall of NGAL in Acute Kidney Injury

Johan Mårtensson, Rinaldo Bellomo (2014)

For many years, neutrophil gelatinase-associated lipocalin (NGAL) has been considered the most promising biomarker of acute kidney injury (AKI). Commercial assays and point-of-care instruments, now available in many hospitals, allow rapid NGAL measurements intended to guide the clinician in the management of patients with or at risk of AKI. However, these assays likely measure a mixture of different NGAL forms originating from different tissues. Systemic inflammation, commonly seen in critically ill patients, and several comorbidities contribute to the release of NGAL from haematopoietic and non-haematopoietic cells. The unpredictable release and complex nature of the molecule and the inability to specifically measure NGAL released by tubular cells have hampered its use a specific marker of AKI in heterogeneous critically ill populations. In this review, we describe the nature and cellular sources of NGAL, its biological role and diagnostic ability in AKI and the increasing concerns surrounding its diagnostic and clinical value.

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Author and article information

Contributors

Johan Mårtensson: +61 3 94965992 , johan.martensson@austin.org.au

Niklas Jonsson: niklas.jonsson@karolinska.se

Neil J. Glassford: neil.glassford@austin.org.au

Max Bell: max.bell@karolinska.se

Claes-Roland Martling: claes-roland.martling@karolinska.se

Rinaldo Bellomo: rinaldo.bellomo@austin.org.au

Anders Larsson: anders.larsson@medsci.uu.se

Journal

Journal ID (nlm-ta): Ann Intensive Care

Journal ID (iso-abbrev): Ann Intensive Care

Title: Annals of Intensive Care

Publisher: Springer Paris (Paris )

ISSN (Electronic): 2110-5820

Publication date (Electronic): 13 January 2016

Publication date PMC-release: 13 January 2016

Publication date Collection: 2016

Volume: 6

Electronic Location Identifier: 6

Affiliations

[ ]Section of Anaesthesia and Intensive Care Medicine, Department of Physiology and Pharmacology, Karolinska Institutet, Solnavägen 1, 171 77 Solna, Sweden

[ ]Department of Intensive Care, Austin Hospital, 145 Studley Road, Heidelberg, VIC 3084 Australia

[ ]Australian and New Zealand Intensive Care Research Centre, School of Preventive Medicine and Public Health, Monash University, The Alfred Centre, 99 Commercial Road, Melbourne, VIC 3004 Australia

[ ]Department of Medical Sciences, Clinical Chemistry, Uppsala University, 751 85 Uppsala, Sweden

Article

Publisher ID: 108

DOI: 10.1186/s13613-016-0108-x

PMC ID: 4712179

PubMed ID: 26762504

SO-VID: 7867ad33-4006-4ab1-9bf1-634bd8d80308

License:

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.