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Updated: Jul 6, 2026

Assessment of Vascular Function in Patients With Chronic Kidney Disease
Published on: June 16, 2014
Serum fetuin-a concentration and endothelial dysfunction in chronic kidney disease
Kayser Caglar1, Mahmut Ilker Yilmaz, Mutlu Saglam
1Department of Nephrology, Gülhane School of Medicine, Ankara, Turkey. kaysercaglar@yahoo.co
Insights
Low fetuin-A levels are linked to endothelial dysfunction in chronic kidney disease (CKD) patients. This suggests fetuin-A may contribute to the development of vascular issues in CKD.
Area of Science:
- Nephrology
- Cardiovascular Medicine
- Biochemistry
Background:
- Endothelial dysfunction is common in chronic kidney disease (CKD) and precedes atherosclerosis.
- Fetuin-A, a known calcification inhibitor, was investigated as a potential factor in endothelial dysfunction.
Purpose of the Study:
- To examine the association between serum fetuin-A concentrations and endothelial dysfunction in patients with varying stages of CKD.
Main Methods:
- 198 non-diabetic CKD patients underwent flow-mediated dilatation (FMD) assessment via brachial ultrasonography.
- Serum fetuin-A levels were measured using ELISA.
- Carotid intima-media thickness was also assessed.
Main Results:
- Endothelial dysfunction was present across all CKD stages and worsened with reduced kidney function.
- Serum fetuin-A levels were decreased in most CKD stages.
- Fetuin-A and intact parathyroid hormone were independently associated with endothelial dysfunction.
Conclusions:
- Fetuin-A may play a role in the development of endothelial dysfunction in patients with chronic kidney disease.
- Further research is warranted to elucidate the precise mechanisms.
Background:
Defective endothelial function, an initial step in the development of atherosclerotic plaque, is prevalent in moderate to advanced chronic kidney disease (CKD). In this study, the investigators hypothesized that fetuin-A, a calcification inhibitor, is a novel risk factor for the development of endothelial dysfunction in patients.
Methods:
198 nondiabetic patients with a mean age of 44.0 +/- 12.4 years and with different stages of CKD were studied. In addition to a detailed metabolic panel, flow-mediated dilatation assessed by high-resolution brachial ultrasonography was performed to determine endothelial dysfunction. Carotid intima-media thickness was also estimated by ultrasonography. Serum fetuin-A concentrations were determined by using a human ELISA method.
Results:
Endothelial dysfunction was observed in all stages (1-5) of CKD and worsened in parallel to the reduction in estimated glomerular filtration rate. Serum fetuin-A concentrations were also found to be decreased in all but stage 1 CKD. On multiple regression analysis, endothelial dysfunction was independently associated with fetuin-A (beta = 0.745, p < 0.001) and intact parathyroid hormone concentrations (beta = -0.216, p < 0.001).
Conclusion:
These data in a selected cohort of CKD patients indicate that fetuin-A may be one of the contributing factors for the development of endothelial dysfunction in CKD patients.
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