Osteocalcin association with vascular function in chronic kidney disease.

J Clin Hypertens (Greenwich)

Department of Nephrology, The First Medical Centre, Chinese PLA General Hospital, Chinese PLA Institute of Nephrology, State Key Laboratory of Kidney Diseases, National Clinical Research Center of Kidney Diseases, Beijing, China.

Published: July 2022


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Article Abstract

Osteocalcin (OCN) is a bone-derived and vitamin K dependent hormone that affects energy metabolism and vascular calcification. The relationship between serum OCN and vascular function in patients with chronic kidney disease (CKD) is uncertain. This study investigated the association between serum OCN and vascular function as expressed with reactive hyperemia index (RHI) and augmentation index (AIx) measured by Endo-PAT 2000 device. This cross-sectional analysis was based on 256 pre-dialysis CKD patients who had completed the Endo-PAT 2000 test and serum OCN at the First Center of Chinese PLA Hospital from November 2017 to December 2019. Based on whether the RHI was less than 1.67, the patients were divided into endothelial dysfunction and normal endothelial function groups. Multiple logistic and linear regression were used to analyze the association between OCN and vascular function. Subgroup analyses were performed to examine the effects of OCN on vascular function in different CKD populations. After multivariate adjustment, CKD with low OCN were more likely to have endothelial dysfunction (OR: 0.794; 95%CI: 0.674-0.934; P = .006); on the contrary, patients with high OCN had a higher degree of arterial stiffness (standardized β: 0.174; P = .003). Subgroup analyses showed that higher OCN was associated with severe arterial stiffness but a better endothelial function in young (age < 65 years, P /P = .027/.011), male (P /P = .040/.016), patients with a history of hypertension (P /P = .004/.009) or diabetes (P /P = .005/.005), and in early CKD (P /P = .014/.015). In conclusion, serum OCN correlates with vascular function in CKD patients: beneficial for endothelial function but detrimental to arterial stiffness.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9278578PMC
http://dx.doi.org/10.1111/jch.14523DOI Listing

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