Publication
Title
Sclerostin : another vascular calcification inhibitor?
Author
Abstract
Context: Sclerostin, a Wnt antagonist produced by osteocytes, regulates osteoblast activity and is a well-established key player in bone turnover. Recent data indicate that the Wnt pathway may also be involved in vascular calcification. Objective: The present study tests the hypothesis that serum sclerostin levels are associated with vascular calcification in patients with chronic kidney disease (CKD) not yet receiving dialysis. Design, Setting, Participants, and Measurements: We performed a cross-sectional analysis in 154 patients with CKD. Aortic calcification (AC) was assessed by lumbar X-ray and scored with a maximum score of 24. In addition to traditional and nontraditional cardiovascular (CV) risk factors, serum sclerostin levels were assessed (ELISA). Regression analysis was performed to identify determinants of serum sclerostin and AC. Results: AC was present in 59% of patients. Older age (P < .0001), male sex (P = .006), lower estimated glomerular rate (eGFR) (P = .0008), lower bone-specific alkaline phosphatase (P = .03), and the absence of AC (P = .006) were identified as independent determinants of higher serum sclerostin levels. In univariate logistic regression, higher age, diabetes, CV history, higher body mass index, higher serum C-reactive protein and sclerostin levels and lower estimated glomerular rate were all associated with the presence of AC. In multivariate analysis, lower, not higher, sclerostin levels (P = .04, odds ratio [OR] per ng/mL of 0.24), higher age (P < .0001, OR per year of 1.17) and CV history (P = .02, OR for a positive CV history of 3.83) were identified as independent determinants of AC. Conclusions: In this cohort of patients with CKD, we found that patients with aortic calcifications (ACs) had higher sclerostin levels. However, in multivariate analysis, the association became inverse. Additional clinical and experimental studies are urgently required to clarify whether or not sclerostin protects against progression of vascular calcification.
Language
English
Source (journal)
The journal of clinical endocrinology and metabolism. - Baltimore, Md
Publication
Baltimore, Md : 2013
ISSN
0021-972X
Volume/pages
98:8(2013), p. 3221-3228
ISI
000322781300038
Full text (Publisher's DOI)
Full text (publisher's version - intranet only)
UAntwerpen
Faculty/Department
Research group
Publication type
Subject
Affiliation
Publications with a UAntwerp address
External links
Web of Science
Record
Identification
Creation 22.08.2013
Last edited 16.11.2017
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