Urinary biomarkers of kidney tubule injury, risk of acute kidney injury, and mortality in patients with acute ischaemic stroke treated at a stroke care unit.


Journal

European journal of neurology
ISSN: 1468-1331
Titre abrégé: Eur J Neurol
Pays: England
ID NLM: 9506311

Informations de publication

Date de publication:
12 2020
Historique:
received: 15 06 2020
accepted: 15 07 2020
pubmed: 23 7 2020
medline: 22 6 2021
entrez: 23 7 2020
Statut: ppublish

Résumé

Urinary liver-type fatty-acid binding protein (L-FABP), which is a biomarker of kidney tubule injury, has been studied extensively and established as a risk marker of acute kidney injury (AKI). The aim of this study was to investigate whether kidney tubule injury is associated with the development of AKI and mortality in patients with acute ischaemic stroke. Acute ischaemic stroke patients hospitalized in the stroke care unit (SCU) within 24 h after symptom onset were prospectively investigated. AKI was defined on the basis of Kidney Disease: Improving Global Outcomes (KDIGO) criteria. Baseline urinary L-FABP was measured on admission. We evaluated the associations among urinary L-FABP, incidence of AKI, and 90-day mortality adjusted for renal function, albuminuria and other potentially predictive variables, using multivariable analysis. In total, 527 acute ischaemic stroke patients (342 men, median age 74 years) were enrolled in the study. Twenty-seven patients (5.1%) experienced AKI within 7 days of admission. In the univariate analysis, high urinary L-FABP level had positive associations with AKI [53.8 μg/g creatinine (Cr) vs. 3.9 μg/g Cr; P < 0.001] and 90-day mortality (15.5 μg/g Cr vs. 4.0 μg/g Cr; P < 0.001). In the multivariate analysis, elevated urinary L-FABP level (per 10-μg/g Cr increase) was independently associated with AKI (odds ratio 1.225, 95% confidence interval (CI) 1.083-1.454; P = 0.003) and 90-day mortality (hazard ratio 1.091, 95% CI 1.045-1.138; P < 0.001). Urinary biomarkers of kidney tubule injury are independently associated with the development of AKI and 90-day mortality in patients with acute ischaemic stroke treated at the SCU.

Sections du résumé

BACKGROUND AND PURPOSE
Urinary liver-type fatty-acid binding protein (L-FABP), which is a biomarker of kidney tubule injury, has been studied extensively and established as a risk marker of acute kidney injury (AKI). The aim of this study was to investigate whether kidney tubule injury is associated with the development of AKI and mortality in patients with acute ischaemic stroke.
METHODS
Acute ischaemic stroke patients hospitalized in the stroke care unit (SCU) within 24 h after symptom onset were prospectively investigated. AKI was defined on the basis of Kidney Disease: Improving Global Outcomes (KDIGO) criteria. Baseline urinary L-FABP was measured on admission. We evaluated the associations among urinary L-FABP, incidence of AKI, and 90-day mortality adjusted for renal function, albuminuria and other potentially predictive variables, using multivariable analysis.
RESULTS
In total, 527 acute ischaemic stroke patients (342 men, median age 74 years) were enrolled in the study. Twenty-seven patients (5.1%) experienced AKI within 7 days of admission. In the univariate analysis, high urinary L-FABP level had positive associations with AKI [53.8 μg/g creatinine (Cr) vs. 3.9 μg/g Cr; P < 0.001] and 90-day mortality (15.5 μg/g Cr vs. 4.0 μg/g Cr; P < 0.001). In the multivariate analysis, elevated urinary L-FABP level (per 10-μg/g Cr increase) was independently associated with AKI (odds ratio 1.225, 95% confidence interval (CI) 1.083-1.454; P = 0.003) and 90-day mortality (hazard ratio 1.091, 95% CI 1.045-1.138; P < 0.001).
CONCLUSION
Urinary biomarkers of kidney tubule injury are independently associated with the development of AKI and 90-day mortality in patients with acute ischaemic stroke treated at the SCU.

Identifiants

pubmed: 32697875
doi: 10.1111/ene.14448
doi:

Substances chimiques

Biomarkers 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

2463-2472

Subventions

Organisme : Japan Society for the promotion of Science
ID : 16K20403

Informations de copyright

© 2020 European Academy of Neurology.

Références

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Auteurs

T Shimoyama (T)

Department of Neurology, Graduate School of Medicine, Nippon Medical School, Tokyo, Japan.

T Sato (T)

Department of Neurology, Graduate School of Medicine, Nippon Medical School, Tokyo, Japan.

Y Sakamoto (Y)

Department of Neurology, Graduate School of Medicine, Nippon Medical School, Tokyo, Japan.

K Nagai (K)

Department of Neurology, Graduate School of Medicine, Nippon Medical School, Tokyo, Japan.

J Aoki (J)

Department of Neurology, Graduate School of Medicine, Nippon Medical School, Tokyo, Japan.

S Suda (S)

Department of Neurology, Graduate School of Medicine, Nippon Medical School, Tokyo, Japan.

Y Nishiyama (Y)

Department of Neurology, Graduate School of Medicine, Nippon Medical School, Tokyo, Japan.

K Kimura (K)

Department of Neurology, Graduate School of Medicine, Nippon Medical School, Tokyo, Japan.

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