Aim: Sclerostin, the protein product of the SOST gene, is a soluble antagonist of the canonical wingless-related integration site (Wnt)-β-catenin pathway. The aim of the study is the relationship between sclerostin and atherosclerosis and arterial stiffness.
Materials and methods: 110 kidney transplant recipients (KTRs) were included in the study. Patients were compared with a control group of 76 healthy individuals matched for age and gender. Renal functions were determined by estimated glomerular filtration rate (eGFR). Atherosclerosis determined by carotid artery intima-media thickness (CAT) and arterial stiffness (AS) determined by brachial-ankle pulse wave velocity (bPWV). Sclerostin levels were determined by an enzyme-related immunosorbent kit. Log10 levels were used due to the dispersed distribution of variables.
Results: CAT, bPWV, and log10 sclerostin were significantly higher and eGFR was significantly lower in patients compared to healthy individuals. In the multivariate analysis, as the CAT value of the patients increased, the probability of having a log10 sclerostin value of 3.8 and above decreased. As the bPWV value of the patients increased, the probability of having a log10 sclerostin value of 3.8 and above decreased.
Conclusion: Increased atherosclerosis, AS development, and increased serum sclerostin levels were detected in KTRs compared to healthy individuals. A significant inverse relationship was found between sclerostin and atherosclerosis and AS. Sclerostin produced in bone and vascular tissue may prevent the development of atherosclerosis and AS.