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. Copyright 2008 S. Karger AG, Basel.
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 nondiabeticpatients 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 CKDpatients indicate that fetuin-A may be one of the contributing factors for the development of endothelial dysfunction in CKDpatients. Copyright 2008 S. Karger AG, Basel.
Authors: Jared M O'Leary; Tufik R Assad; Meng Xu; Kelly A Birdwell; Eric Farber-Eger; Quinn S Wells; Anna R Hemnes; Evan L Brittain Journal: Pulm Circ Date: 2017-06-29 Impact factor: 3.017
Authors: N P Nickel; J M O'Leary; E L Brittain; J P Fessel; R T Zamanian; J D West; E D Austin Journal: Pulm Circ Date: 2017-03-13 Impact factor: 3.017