Soluble interleukin-2 receptor predicts acute kidney injury and in-hospital mortality in patients with acute myocardial infarction.


Journal

International journal of cardiology
ISSN: 1874-1754
Titre abrégé: Int J Cardiol
Pays: Netherlands
ID NLM: 8200291

Informations de publication

Date de publication:
01 10 2023
Historique:
received: 13 03 2023
revised: 24 06 2023
accepted: 05 07 2023
medline: 14 8 2023
pubmed: 10 7 2023
entrez: 9 7 2023
Statut: ppublish

Résumé

Acute kidney injury (AKI) is the most common and critical complication in patients with acute myocardial infarction (AMI). This study aims to evaluate the significance of elevated soluble interleukin 2 receptor (sIL-2R) levels in predicting AKI and mortality. A total of 446 patients with AMI were enrolled between January 2020 and July 2022, including 58 patients with AKI and 388 without AKI. The sIL-2R levels were measured using a commercially available chemiluminescence enzyme immunoassay. Logistic regression analysis was used to examine the risk factors for AKI. Discrimination was assessed based on the area under the receiver operating characteristic curve. The model was internally validated using 10-fold cross-validation. During hospitalization, 13% of patients developed AKI following AMI, with higher sIL-2R levels (0.61 ± 0.27 U/L vs. 0.42 ± 0.19 U/L, p = 0.003) and in-hospital all-cause mortality (12.1% vs. 2.6%, P < 0.001). The sIL-2R levels emerged as an independent risk factor for both AKI (OR = 5.08, 95% CI (1.04-24.84, p < 0.045) and in-hospital all-cause mortality (OR = 73.57,95% CI 10.24-528.41, p < 0.001) in AMI patients. The sIL-2R levels were found to be useful biomarkers in prediction of AKI and in-hospital all-cause mortality in patients with AMI (AUC: 0.771 and 0.894, respectively). The respective cutoff values for sIL-2R levels in predicting AKI and in-hospital all-cause mortality were determined to be 0.423 U/L and 0.615 U/L. The level of sIL-2R was an independent risk factor and predictor for both AKI and in-hospital all-cause mortality in patients with AMI. These findings highlight the potential of sIL-2R as a valuable tool for identifying high-risk patients regarding AKI and in-hospital mortality.

Sections du résumé

BACKGROUND
Acute kidney injury (AKI) is the most common and critical complication in patients with acute myocardial infarction (AMI). This study aims to evaluate the significance of elevated soluble interleukin 2 receptor (sIL-2R) levels in predicting AKI and mortality.
METHODS
A total of 446 patients with AMI were enrolled between January 2020 and July 2022, including 58 patients with AKI and 388 without AKI. The sIL-2R levels were measured using a commercially available chemiluminescence enzyme immunoassay. Logistic regression analysis was used to examine the risk factors for AKI. Discrimination was assessed based on the area under the receiver operating characteristic curve. The model was internally validated using 10-fold cross-validation.
RESULTS
During hospitalization, 13% of patients developed AKI following AMI, with higher sIL-2R levels (0.61 ± 0.27 U/L vs. 0.42 ± 0.19 U/L, p = 0.003) and in-hospital all-cause mortality (12.1% vs. 2.6%, P < 0.001). The sIL-2R levels emerged as an independent risk factor for both AKI (OR = 5.08, 95% CI (1.04-24.84, p < 0.045) and in-hospital all-cause mortality (OR = 73.57,95% CI 10.24-528.41, p < 0.001) in AMI patients. The sIL-2R levels were found to be useful biomarkers in prediction of AKI and in-hospital all-cause mortality in patients with AMI (AUC: 0.771 and 0.894, respectively). The respective cutoff values for sIL-2R levels in predicting AKI and in-hospital all-cause mortality were determined to be 0.423 U/L and 0.615 U/L.
CONCLUSIONS
The level of sIL-2R was an independent risk factor and predictor for both AKI and in-hospital all-cause mortality in patients with AMI. These findings highlight the potential of sIL-2R as a valuable tool for identifying high-risk patients regarding AKI and in-hospital mortality.

Identifiants

pubmed: 37423564
pii: S0167-5273(23)00963-4
doi: 10.1016/j.ijcard.2023.131156
pii:
doi:

Substances chimiques

Biomarkers 0
Receptors, Interleukin-2 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

131156

Informations de copyright

Copyright © 2023 Elsevier B.V. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of Competing Interest The authors declare that they have no conflicts of interest.

Auteurs

Jianquan Liao (J)

Department of Cardiology, Zhongshan Hospital, Fudan University, Shanghai Institute of Cardiovascular Diseases, Shanghai, China.

Meng Zhang (M)

Department of Cardiology, Zhongshan Hospital, Fudan University (Xiamen Branch), Xiamen, Fujian, China.

Rende Xu (R)

Department of Cardiology, Zhongshan Hospital, Fudan University, Shanghai Institute of Cardiovascular Diseases, Shanghai, China.

Runda Wu (R)

Department of Cardiology, Zhongshan Hospital, Fudan University, Shanghai Institute of Cardiovascular Diseases, Shanghai, China.

Huairui Shi (H)

Department of Cardiology, Zhongshan Hospital, Fudan University, Shanghai Institute of Cardiovascular Diseases, Shanghai, China.

Qi Jin (Q)

Department of Cardiology, Zhongshan Hospital, Fudan University, Shanghai Institute of Cardiovascular Diseases, Shanghai, China.

Yi Fang (Y)

Department of Nephrology, Zhongshan Hospital, Fudan University, Shanghai, China.

Jiarui Xu (J)

Department of Nephrology, Zhongshan Hospital, Fudan University, Shanghai, China. Electronic address: xu.jiarui@zs-hospital.sh.cn.

Kang Yao (K)

Department of Cardiology, Zhongshan Hospital, Fudan University, Shanghai Institute of Cardiovascular Diseases, Shanghai, China. Electronic address: yao.kang@zs-hospital.sh.cn.

Yeqing Xie (Y)

Department of Nephrology, Zhongshan Hospital, Fudan University, Shanghai, China. Electronic address: xie.yeqing@zs-hospital.sh.cn.

Junbo Ge (J)

Department of Cardiology, Zhongshan Hospital, Fudan University, Shanghai Institute of Cardiovascular Diseases, Shanghai, China. Electronic address: jbge@zs-hospital.sh.cn.

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Classifications MeSH