Abstract
Sclerostin (SOST gene product) is a circulating inhibitor of Wnt/-cathenin signaling pathway, secreted mainly by osteocytes. Sclerostin has negative effect on osteoblastogenesis, thereby inhibits bone formation and significantly contributes to the development of osteoporosis.
Chronic kidney disease (CKD) is associated with calcium, phosphorus and vitamin D metabolism disorders and it is obligatory connected with renal osteopathy and cardiovascular system disorders (chronic kidney disease - mineral and bone disorder, CKD-MBD). According to recent studies sclerostin could be a link which takes part in communication between vessel walls and bones (bone-vascular cross-talk).
Serum sclerostin concentration increases in the course of chronic kidney disease. Not only missing renal elimination, but also bone metabolism change, i.e. sclerostin secretion change, could be the reason.
Contrary to the expectations, correlation between bone density and sclerostin serum concentration is rather positive than negative, which can also show a change between sclerostin secretion and elimination in CKD patients. Inverse correlation between parathormone and sclerostin is preserved in CKD patients, even those with end stage renal disease.
It could be hypothesized, that sclerostin can play a role in the pathogenesis of adynamic bone disease in these patients. The prognostic relevance of sclerostin is intensively studied in CKD patients, especially those on long-term maintenance haemodialysis (HD).
Some recent studies show, that high sclerostin levels in HD patients predict lower cardiovascular mortality of these patients. Rather hypothetical explanation is possible protective effect of sclerostin on the vascular wall, but more studies must be done to prove this.
The goal of this article is to summarize previous knowledge about sclerostin, especially in CKD and HD patients.