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NDT Advance Access originally published online on April 27, 2006
Nephrology Dialysis Transplantation 2006 21(8):2144-2151; doi:10.1093/ndt/gfl204
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© The Author [2006]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Original Articles: Clinical Nephrology

Fetuin-A and kidney function in persons with coronary artery disease—data from the heart and soul study

Joachim H. Ix1,2, Glenn M. Chertow1,2,3, Michael G. Shlipak2,3,4, Vincent M. Brandenburg5, Markus Ketteler5 and Mary A. Whooley2,3,4

1 Division of Nephrology, 2 Department of Medicine, 3 Department of Epidemiology and Biostatistics, University of California, San Francisco, 4 Section of General Internal Medicine, VA Medical Center, San Francisco, CA, USA, and 5 Department of Nephrology and Clinical Immunology, University Hospital of the RWTH, Aachen, Aachen, Germany

Correspondence and offprint requests to: Joachim H. Ix, MD, Division of Nephrology, Department of Medicine, Box 0532, HSE 672, University of California, San Francisco, San Francisco, CA 94143-0532, USA. Email: jix{at}medicine.ucsf.edu

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 m2, and 0.65 g/l in participants with CrCl < 45 ml/min/1.73 m2. 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.

Keywords: calcium; chronic kidney disease; fetuin-A; alpha-2-Heremans-Schmid-glycoprotein; vascular calcification; phosphorus


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