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The Relationship of Fetuin-A with Coronary Calcification, Carotid Atherosclerosis, and Mortality Risk in Non-Dialysis
Osama Nady Mohamed1, Mahmoud Ragab Mohamed Mohamed1, Israa Gamal Hassan1
1Department of Internal Medicine, Faculty of Medicine, Minia University, Minya, Egypt.
Insights
Fetuin-A levels are lower in non-dialysis chronic kidney disease (CKD) patients and predict coronary artery calcification (CAC) and carotid atherosclerosis. Low fetuin-A and CAC are significant risk factors for mortality in CKD.
Area of Science:
- Nephrology
- Cardiology
- Biochemistry
Background:
- Chronic kidney disease (CKD) is associated with increased cardiovascular risk.
- Biomarkers predicting cardiovascular complications in non-dialysis CKD patients are crucial for risk stratification.
Purpose of the Study:
- To investigate the association of fetuin-A with coronary artery calcification (CAC), carotid atherosclerosis, and mortality in non-dialysis CKD patients.
- To determine if fetuin-A predicts cardiovascular events and mortality in this population.
Main Methods:
- Study included 135 adult patients with CKD stages 3-5, excluding smokers, diabetics, and those with inflammatory conditions, liver disease, acute kidney failure, hemodialysis, or cancer.
- Evaluated serum levels of fetuin-A, inflammatory markers (TNF-α, hs-CRP, IL-6), lipids, PTH, and phosphorus.
- Assessed coronary artery calcification (CAC) using cardiac spiral CT (Agatston method) and carotid atherosclerosis (IMT, plaques) via ultrasonography.
Main Results:
- Patients with CAC exhibited significantly higher levels of inflammatory markers, lipids, PTH, and phosphorus, and lower levels of fetuin-A compared to non-CAC patients (p<0.001).
- Fetuin-A levels decreased with CKD progression.
- Fetuin-A, age, inflammatory markers, lipids, PTH, and phosphorus were significant predictors of CAC. Both CAC and fetuin-A strongly predicted all-cause and cardiovascular mortality. Fetuin-A also predicted carotid intima-media thickness (CIMT).
Conclusions:
- Fetuin-A is a reliable predictor of coronary artery calcification and carotid atherosclerosis in non-dialysis CKD.
- Fetuin-A and CAC are significant risk factors for all-cause and cardiovascular mortality in patients with non-dialysis CKD.
Objective:
This study investigated the relationship of fetuin-A with coronary calcification, carotid atherosclerosis, and mortality risk in non-dialysis chronic kidney disease (CKD).
Methods:
The study included 135 adult patients with CKD at stages 3-5, who were divided into coronary artery calcification (CAC) and non-CAC groups. We excluded current smokers and individuals with diabetes mellitus, inflammatory conditions, liver diseases, acute kidney failure, chronic hemodialysis, and cancer. We conducted kidney function tests, complete blood counts, and measured serum levels of fetuin-A, tumor necrosis factor-alpha (TNF-α), high-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6), total cholesterol (TC), total triglycerides (TG), high-density lipoprotein cholesterol, and low-density lipoprotein cholesterol. Cardiac spiral computed tomography was used to calculate the CAC score, employing the Agatston method. Carotid ultrasonography was performed to assess carotid intima-media thickness (CIMT) and to detect the presence of plaques.
Results:
CAC patients had considerably higher levels of TNF-α (p<0.001), IL-6 (p<0.001), hs-CRP (p=0.006), TC, TG, parathyroid hormone (PTH) (p<0.001) and phosphorus (p<0.001) than non-CAC patients. They also had significantly lower levels of fetuin-A (p<0.001). Fetuin-A was considerably lower in CKD subgroups as CKD progressed. Fetuin-A (p=0.046), age (p=0.009), TNF-α (p=0.027), IL-6 (p=0.005), TG (p=0.002), PTH (p=0.002), and phosphorus (p=0.004) were significant predictors of CAC. CAC and fetuin-A were strong predictors of all-cause mortality and cardiovascular (CV) mortality. Fetuin-A was a significant predictor of CIMT (p=0.045).
Conclusion:
Fetuin-A reliably predicted CAC and CIMT. Fetuin-A and CAC emerged as significant risk factors for all-cause and CV mortality in non-dialysis CKD.
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