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Nephron Clin Pract. 2008;108(3):c233-40. doi: 10.1159/000120209. Epub 2008 Mar 11.

Serum fetuin-a concentration and endothelial dysfunction in chronic kidney disease.

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  • 1Department of Nephrology, G├╝lhane School of Medicine, Ankara, Turkey.



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.


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.


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).


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.

Copyright 2008 S. Karger AG, Basel.

[PubMed - indexed for MEDLINE]
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