Relationship between sclerostin and cardiovascular calcification in hemodialysis patients: a cross-sectional study

Brandenburg, Vincent; Kramann, Rafael; Koos, Ralf; Krüger, Thilo; Schurgers, Leon J.; Mühlenbruch, Georg; Hübner, Sinah; Gladziwa, U.; Drechsler, Christiane; Ketteler, Markus

doi:10.1186/1471-2369-14-219

Cited by 146 publications

(150 citation statements)

References 35 publications

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“…45,46 Resulting from experimental data, these hypotheses were not tested in this population, but serum sclerostin is increased in patients with ESRD 47,48 and associated with cardiovascular calcifications. 49 Our findings support, in a human ESRD population, the common role of inflammation in bone and cardiovascular remodeling, which was shown experimentally by Hjortnaes et al, 24 but the association between low bone turnover and arterial remodeling is not new. 8,50 Hjortnaes et al 24 confirm the dissociation between serum PTH concentrations and bone histology and PTH concentration with clinical disease.…”

Section: Discussionsupporting

confidence: 87%

Ankle-Brachial Index and Bone Turnover in Patients on Dialysis

London

Marchais²,

Guérin

et al. 2015

Journal of the American Society of Nephrology

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An association between atherosclerosis and osteoporosis has been reported in several studies. This association could result from local intraosseous atherosclerosis and ischemia, which is shown by limb osteoporosis in patients with peripheral artery disease (PAD), but also could result from bidirectional communication between the skeleton and blood vessels. Systemic bone disorders and PAD are frequent in ESRD. Here, we investigated the possible interaction of these disorders. For 65 prevalent nondiabetic patients on hemodialysis, we measured ankle-brachial pressure index (ABix) and evaluated mineral and bone disorders with bone histomorphometry. In prevalent patients on hemodialysis, PAD (ABix,0.9 or .1.4/incompressible) was associated with low bone turnover and pronounced osteoblast resistance to parathyroid hormone (PTH), which is indicated by decreased double-labeled surface and osteoblast surface (P,0.001). Higher osteoblast resistance to PTH in patients with PAD was characterized by weaker correlation coefficients (slopes) between serum PTH and double-labeled surface (P=0.02) or osteoblast surface (P=0.03). The correlations between osteoclast number or eroded surface and serum mineral parameters, including PTH, did not differ for subjects with normal ABix and PAD. Common vascular risk factors (dyslipidemia, smoking, and sex) were similar for normal, low, and incompressible ABix. Patients with PAD were older and had high C-reactive protein levels and longer hemodialysis vintage. These results indicate that, in prevalent nondiabetic patients with ESRD, PAD associates with low bone turnover and pronounced osteoblast resistance to PTH.

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Section: Discussionsupporting

confidence: 87%

Ankle-Brachial Index and Bone Turnover in Patients on Dialysis

London

Marchais²,

Guérin

et al. 2015

Journal of the American Society of Nephrology

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“…In the future, these data will be repeatedly confirmed by the results of other studies devoted to identify the role of sclerostin in patients on regular haemodialysis [23,49].…”

Section: The Relation Of Fgf-23 Klotho and Sclerostin With Cardiovassupporting

confidence: 64%

“…In recent years, data on the important role of sclerostin glycoprotein in CKD are accumulating [22,23]. Sclerostin, synthesized by osteocytes, blocks Wnt signalling pathway that leads to suppression of bone formation, as a result of decreased osteoblast differentiation and proliferation and osteocyte apoptosis [24].…”

Section: Introductionmentioning

confidence: 99%

“…It is important to determine the clinical significance of changes in sclerostin metabolism in CKD, because the relationship between adynamic bone disease (ABD) and calcification of the heart and blood vessels in patients with CKD is considered proven [27]. At the same time, available-to-date publications on the role of sclerostin in ectopic calcification still remain contradictory [22,23,25,26].…”

Section: Introductionmentioning

confidence: 99%

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Disorders in the System of Mineral and Bone Metabolism Regulators—FGF-23, Klotho and Sclerostin—in Chronic Kidney Disease: Clinical Significance and Possibilities for Correction

Milоvаnоvа¹,

Fоmin²,

Lysenko³

et al. 2018

Chronic Kidney Disease - From Pathophysiology to Clinical Improvements

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The chapter discusses the current understanding of the system of mineral and bone metabolism regulators-FGF-23, Klotho and sclerostin-disturbances in chronic kidney disease (CKD). In the chapter we presented the date, including our own results, which allow to suggest the change in the ratio of FGF-23-Klotho-sclerostin in CKD as an early biomarker not only for the chronic kidney damage but also for high cardiovascular (CV) risk. Results of studies show that disorders in FGF-23-Klotho-sclerostin ratio correlate with the frequency and severity of hypertension, vascular calcification, cardiac remodelling, anaemia, malnutrition, inflammation and strong aggravate CV risk in CKD. It was found independent from blood pressure (BP) action of increased serum FGF-23 on the myocardium as well as the correlation of serum high-sensitive troponin I with increased serum FGF-23 and low Klotho levels in CKD patients. At the same time, it was shown that renoprotective therapy, including renin-angiotensin blockers, low-protein diet with amino/keto acid supplementation and phosphate binders, erythropoiesis stimulators, vitamin D metabolites used to get the target levels of BP, serum phosphorus, haemoglobin, parathyroid hormone and nutritional status disorders correction can reduce the risk of CV events, as the major cause of death in CKD patients.

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“…Sclerostin is constitutively expressed in the aorta [16][17][18] and up-regulated in foci of vascular and valvular calcification. [19][20][21][22] The function of sclerostin in the vasculature is unknown. Although sclerostin may function as a negative regulator of vascular calcification and sclerostin inhibition could promote vascular calcification, studies have shown conflicting results.…”

Section: Discussionmentioning

confidence: 99%