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Sclerostin in a context of chronic kidney disease (Review)

Abstract

Disarrangement of bone metabolism and vascular calcification significantly contribute to the development of cardiovascular complications in patients with reduced kidney function, thereby determining the worst survival in this group of patients. In recent years, more attention has been paid to search and research of markers of bone damage that are associated with the development of a number of systemic complications in patients with chronic kidney disease, including patients on renal replacement therapy. Wnt-signaling pathway consists of a number of complex proteins, constantly interacting with each other and determining not only normal embryogenesis, but also bone metabolism. Sclerostin by inhibiting Wnt-signaling pathway alters bone formation by suppressing the proliferation and differentiation of osteoblasts. Patients with impaired renal function have elevated serum levels of sclerostin due to its enhanced synthesis. However, until now it is not known whether sclerostin is a predictor of poor prognosis in patients with CKD, or it acts as a kind of protector of vascular wall from calcification, thus ensuring a better survival of both vascular access and patients in general. The review presents recent data on a role of sclerostin in bone metabolism, its participation in the processes of bone remodeling in patients with renal insufficiency, as well as potential therapeutic strategies aimed at changing the concentration of the protein.

About the Author

E. A. Gurevich
University Hospital, Zurich, Switzerland
Russian Federation


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Gurevich E.A. Sclerostin in a context of chronic kidney disease (Review). Nephrology and Dialysis. 2014;16(3):339-349. (In Russ.)

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