Can plasma TWEAK levels predict coronary slow flow in patients with chronic kidney disease?


Journal

The American journal of the medical sciences
ISSN: 1538-2990
Titre abrégé: Am J Med Sci
Pays: United States
ID NLM: 0370506

Informations de publication

Date de publication:
11 2022
Historique:
received: 25 12 2020
revised: 23 07 2021
accepted: 02 05 2022
pubmed: 12 5 2022
medline: 25 10 2022
entrez: 11 5 2022
Statut: ppublish

Résumé

The tumor necrosis factor-like weak inducer of apoptosis (TWEAK) is one of the inflammatory mediators contributing to the atherosclerotic process. TWEAK has been studied in patients with chronic kidney disease (CKD), and it has demonstrated that its level declines as estimated glomerular filtration rate (eGFR) decreases. Most studies have found that the decreased TWEAK levels were seen in atherosclerosis and associated with plaque calcification. The objective of this prospective study was to clarify any relationship between coronary slow-flow (CSF) and TWEAK levels in patients with CKD under conservative treatment. This prospective study included 93 consecutive patients with CKD (mean creatinine level was 1.8±0.4 mg/dL) undergoing invasive coronary angiography (ICA) for any reason except for acute coronary syndromes from May 2019 to March 2020. A total of 93 patients were divided into two groups concerning having CSF (n=35) or no-CSF (n=58). Patients with CSF had higher TWEAK levels than those without CSF (695.2± 225.2 vs. 465.8±157.6, p<0.001). As the number of coronary arteries with slow flow increased, TWEAK levels increased statistically significantly (r:0.635/ p<0.001). Receiver operating characteristic (ROC) analysis showed that TWEAK levels of 516 pg/mL could predict CSF in patients with CKD. Our study has shown that plasma TWEAK levels were an independent predictor for CSF in patients with CKD. In addition, our study has found that elevated TWEAK levels may not reflect the healthy arteries as it was hypothesized in the past.

Sections du résumé

BACKGROUND
The tumor necrosis factor-like weak inducer of apoptosis (TWEAK) is one of the inflammatory mediators contributing to the atherosclerotic process. TWEAK has been studied in patients with chronic kidney disease (CKD), and it has demonstrated that its level declines as estimated glomerular filtration rate (eGFR) decreases. Most studies have found that the decreased TWEAK levels were seen in atherosclerosis and associated with plaque calcification. The objective of this prospective study was to clarify any relationship between coronary slow-flow (CSF) and TWEAK levels in patients with CKD under conservative treatment.
METHODS
This prospective study included 93 consecutive patients with CKD (mean creatinine level was 1.8±0.4 mg/dL) undergoing invasive coronary angiography (ICA) for any reason except for acute coronary syndromes from May 2019 to March 2020. A total of 93 patients were divided into two groups concerning having CSF (n=35) or no-CSF (n=58).
RESULTS
Patients with CSF had higher TWEAK levels than those without CSF (695.2± 225.2 vs. 465.8±157.6, p<0.001). As the number of coronary arteries with slow flow increased, TWEAK levels increased statistically significantly (r:0.635/ p<0.001). Receiver operating characteristic (ROC) analysis showed that TWEAK levels of 516 pg/mL could predict CSF in patients with CKD.
CONCLUSIONS
Our study has shown that plasma TWEAK levels were an independent predictor for CSF in patients with CKD. In addition, our study has found that elevated TWEAK levels may not reflect the healthy arteries as it was hypothesized in the past.

Identifiants

pubmed: 35545142
pii: S0002-9629(22)00217-8
doi: 10.1016/j.amjms.2022.05.003
pii:
doi:

Substances chimiques

Biomarkers 0
Creatinine AYI8EX34EU
Inflammation Mediators 0
TNFSF12 protein, human 0

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

595-600

Informations de copyright

Copyright © 2022 Southern Society for Clinical Investigation. Published by Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of Competing Interest All authors declared no potential conflicts of interest concerning the research, authorship, and publication of this article.

Auteurs

Mustafa A Tatlisu (MA)

Department of Cardiology, Istanbul Medeniyet University Faculty of Medicine, Istanbul, 34722, Turkey. Electronic address: adem.tatlisu@medeniyet.edu.tr.

Adem Atici (A)

Department of Cardiology, Istanbul Medeniyet University Faculty of Medicine, Istanbul, 34722, Turkey.

Fatma Betul Ozcan (FB)

Department of Cardiology, Istanbul Medeniyet University Faculty of Medicine, Istanbul, 34722, Turkey.

Eray Kirac (E)

Department of Biochemistry, Istanbul Medeniyet University Faculty of Medicine, Istanbul, 34722, Turkey.

Omer Faruk Baycan (OF)

Department of Cardiology, Istanbul Medeniyet University Faculty of Medicine, Istanbul, 34722, Turkey.

Mustafa Caliskan (M)

Department of Cardiology, Istanbul Medeniyet University Faculty of Medicine, Istanbul, 34722, Turkey.

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Classifications MeSH