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Updated: May 25, 2026
Assessment of Vascular Function in Patients With Chronic Kidney Disease
Published on: June 16, 2014
Soluble TWEAK and cardiovascular morbidity and mortality in chronic kidney disease patients
Seham Bakry Hassan1, Ahmed Bahgat El-demery, Asmaa Ismail Ahmed
1Department of Internal Medicine, Cairo University, Egypt. sehambakry@yahoo.com
Insights
Soluble TWEAK (sTWEAK) is a potential biomarker for cardiovascular disease in chronic kidney disease (CKD) patients. Lower sTWEAK levels indicate higher cardiovascular risk and atherosclerosis in CKD.
Area of Science:
- Nephrology
- Cardiology
- Biomarkers
Background:
- Cardiovascular disease (CVD) poses a significant threat to patients with chronic kidney disease (CKD).
- Identifying reliable biomarkers for CVD risk in CKD is crucial for patient outcomes.
Purpose of the Study:
- To investigate the role of soluble tumor necrosis factor (TNF) weak inducer of apoptosis (sTWEAK) as a marker for cardiovascular morbidity and mortality in CKD patients.
- To assess the relationship between sTWEAK levels, atherosclerosis markers, and cardiovascular events in CKD.
Main Methods:
- Studied 75 CKD patients across different stages (1-5) and 20 controls.
- Measured serum levels of interleukin-6 (IL-6) and sTWEAK using ELISA and chemiluminescent assays.
- Assessed carotid intima-media thickness (IMT) and followed patients for cardiovascular events over two years.
Main Results:
- IL-6 levels were highest in advanced CKD, while sTWEAK levels were lowest.
- sTWEAK showed a strong negative correlation with IL-6 and IMT.
- CKD patients who developed cardiovascular events (ischemic heart disease, stroke, peripheral arterial disease) had significantly lower baseline sTWEAK levels.
Conclusions:
- Soluble TWEAK (sTWEAK) shows promise as a novel biomarker for atherosclerosis and endothelial dysfunction in CKD.
- Low sTWEAK levels are associated with increased cardiovascular risk and adverse outcomes in CKD patients.
Introduction:
Cardiovascular disease (CVD) is a major cause of morbidity and mortality in chronic kidney patients (CKD). The aim of this study was to demonstrate the role of soluble tumor necrosis factor (TNF) weak inducer of apoptosis (sTWEAK) as a marker of cardiovascular morbidity and mortality in CKD patients.
Methods:
The study included 75 CKD patients classified according to eGFR into three groups; group-1 included 15 patients with stage-1 CKD, group-2 included 30 patients with stage-2 and stage-3 CKD, and group-3 included 30 patients with stage-4 and stage-5 CKD. The three groups were compared to 20 matched controls. Interleukin-6 (IL-6) and sTWEAK were measured using ELISA and chemiluminescent techniques respectively. Carotid intima-media thickness (IMT) was also measured.
Results:
We found that IL-6 showed significant difference between patient groups and controls, being highest in stage 4 and 5 CKD patients and lowest in controls. Soluble TWEAK showed significant difference between patient groups and controls, being lowest in stage 4 and 5 CKD patients and highest in controls. Soluble TWEAK level showed significant negative correlation with IL-6 (r = -0.68; P < 0.01) and carotid IMT (r = -0.95; P < 0.01). After two years follow up, nine out of 75 CKD patients developed ischemic heart disease (IHD). Two patients developed cerebrovascular stroke and another patient developed peripheral arterial disease. These patients had significantly lower levels of sTWEAK at baseline compared to other patients (160.5 ± 60.2 versus 274.8 ± 90 pg/mL; P < 0.05).
Conclusion:
Soluble TWEAK can be a novel biomarker of atherosclerosis and endothelial dysfunction as well as cardiovascular outcome in CKD patients.
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