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Association of serum fetuin‐A with carotid arterial stiffness
Author(s) -
Mori Katsuhito,
Emoto Masanori,
Araki Takahiro,
Yokoyama Hisayo,
Teramura Megumi,
Lee Eiko,
Motoyama Koka,
Koyama Hidenori,
Shoji Tetsuo,
Inaba Masaaki,
Nishizawa Yoshiki
Publication year - 2007
Publication title -
clinical endocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.055
H-Index - 147
eISSN - 1365-2265
pISSN - 0300-0664
DOI - 10.1111/j.1365-2265.2006.02716.x
Subject(s) - fetuin , medicine , arterial stiffness , cardiology , calcification , endocrinology , blood pressure , glycoprotein , biology , microbiology and biotechnology
Summary Objective Fetuin‐A is a circulating glycoprotein which is well characterized as an inhibitor of ectopic calcification. Vascular calcification commonly found in chronic kidney disease (CKD) patients is a predictor of cardiovascular death. Recently, several groups have demonstrated that low fetuin‐A levels are associated with mortality in uraemic patients, possibly through regulation of vascular calcification. However, the physiological significance of fetuin‐A in atherosclerosis remains unknown, except in specific conditions, such as vascular calcification in CKD patients. The objective of this study was to investigate the association between serum fetuin‐A levels and arterial stiffness, a functional property of atherosclerosis, in healthy subjects. Patients and measurements The study subjects comprised 141 healthy subjects. We measured serum fetuin‐A levels and stiffness parameter β for the common carotid artery, which was assessed by ultrasound using a phase‐locked echo‐tracking system. Results Simple regression analyses indicated that serum fetuin‐A levels were significantly correlated with stiffness parameter β ( r = 0·200, P = 0·018). Multiple regression analyses showed that, besides age, fetuin‐A (β = 0·166, P = 0·033) independently contribute to the stiffness parameter β ( R 2 = 0·310, P < 0·0001). Conclusions Serum fetuin‐A level is associated with carotid arterial stiffness, independent of known atherogenic factors in healthy subjects.