Radial artery sclerostin expression in chronic kidney disease stage 5 predialysis patients: a cross-sectional observational study.

Abstract

Bone metabolism disorder is often associated with cardiovascular calcification in patients with chronic kidney disease (CKD). Sclerostin, a novel candidate protein, has been identified to be involved in the bone-vascular axis. The aims of the current investigation were to assess vessel sclerostin expression and its relationship with circulating sclerostin levels. A cross-sectionalobservational study was conducted from January 2012 to December 2014. Thirty-two predialysis patients with CKD stage 5 who received arteriovenous fistula (AVF) operations were enrolled in this study. Radial arteries were collected and paraffin-embedded during the AVF operation, followed by immunohistochemical staining for sclerostin expression. In addition, serum sclerostin levels were measured by the enzyme-linked immunosorbent assay. The prevalence of positive sclerostin staining in the radial arteries was 56.25%. Sclerostin expression was localized in the artery media layer. Serum sclerostin levels in patients with positive sclerostin expression were much higherthan in those with negative expression (p=0.018). Multivariate logistic regression analyses including potential confounders as age, gender, systolic blood pressure (BP), diastolic BP, serum sclerostin, corrected calcium (Ca), phosphate (P), Ca×P product, alkaline phosphatase, intact parathyroid hormone, and estimated glomerular filtration rate showed that only serum sclerostin levels were closely related to vessel sclerostin expression (p=0.025). The area under the curve of serum sclerostin levels for predicting positive vessel sclerostin expression was 0.742 with 61.1% sensitivity and 85.7% specificity (p =0.008). The cutoff point for vessel sclerostin expression of serum sclerostin was 1591.53pg/mL. Positive expression of sclerostin in the radial artery media layer was related to high serum sclerostin levels. Sclerostin may act as both a local and systemic regulator involved in vascular calcification.