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Updated: Aug 9, 2026

Assessment of Vascular Function in Patients With Chronic Kidney Disease
Published on: June 16, 2014
Fetuin-A and kidney function in persons with coronary artery disease--data from the Heart and Soul Study
Joachim H Ix1, Glenn M Chertow, Michael G Shlipak
1Division of Nephrology, Department of Medicine, Box 0532, HSE 672, University of California, San Francisco, San Francisco, CA 94143-0532, USA. jix@medicine.ucsf.edu
Insights
Serum fetuin-A concentrations do not decrease with mild-to-moderate chronic kidney disease (CKD). This study found no association between reduced kidney function and lower fetuin-A levels in patients with coronary artery disease.
Area of Science:
- Nephrology
- Cardiology
- Biochemistry
Background:
- Fetuin-A inhibits vascular calcification and is lower in end-stage renal disease.
- The relationship between fetuin-A and mild-to-moderate chronic kidney disease (CKD) is not well understood.
Purpose of the Study:
- To investigate the association between serum fetuin-A concentrations and varying stages of kidney function in patients with coronary artery disease.
Main Methods:
- Evaluated 970 outpatients with coronary artery disease.
- Assessed kidney function using creatinine clearance (CrCl), estimated glomerular filtration rate (GFR), cystatin-C, and albumin-to-creatinine ratio.
- Utilized general linear models to analyze adjusted mean fetuin-A concentrations across kidney function categories.
Main Results:
- No significant differences in mean fetuin-A concentrations were observed across groups defined by CrCl, GFR, or albumin-to-creatinine ratio.
- Higher serum cystatin-C levels, indicating poorer kidney function, were associated with higher adjusted mean serum fetuin-A concentrations (P for trend <0.001).
Conclusions:
- Mild-to-moderate CKD is not associated with lower serum fetuin-A concentrations in ambulatory patients with coronary artery disease.
- The mechanisms linking CKD and vascular calcification require further investigation.
Background:
Fetuin-A is a serum protein that inhibits ectopic vascular calcification and is present in lower concentrations in end-stage renal disease than in healthy controls. Whether fetuin-A concentrations are also lower in the setting of mild-to-moderate chronic kidney disease (CKD) is unknown.
Methods:
We evaluated the associations of several parameters of kidney function including measured 24 h urinary creatinine clearance (CrCl), estimated glomerular filtration rate (GFR) by the Mayo Clinic quadratic GFR equation (qGFR), serum cystatin-C concentrations, and urinary albumin-to-creatinine ratio with serum fetuin-A concentrations in 970 outpatients with coronary artery disease. We used general linear models to determine the adjusted mean fetuin-A concentrations within each kidney function category.
Results:
The mean age of the study sample was 67 years, 82% were male, 71% had hypertension and 26% had diabetes mellitus. In adjusted analysis, we observed no significant differences in mean fetuin-A concentrations across groups defined by CrCl, qGFR, or albumin-to-creatinine ratio groups. For example, adjusted mean fetuin-A concentrations were 0.66 g/l in participants with CrCl > 90, 60-90 and 45-60 ml/min/1.73 m(2), and 0.65 g/l in participants with CrCl < 45 ml/min/1.73 m(2). Higher serum cystatin-C (indicating worse kidney function) was associated with higher adjusted mean serum fetuin-A concentrations (lowest quartile 0.62 g/l, highest quartile 0.68 g/l; P for trend <0.001).
Conclusions:
Among ambulatory patients with coronary artery disease, there is no evidence that mild-to-moderate CKD is associated with lower concentrations of serum fetuin-A compared with persons with normal renal function. The mechanisms explaining the association between CKD and vascular calcification remain elusive.
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