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Published on: June 2, 2022
Relationship between sclerostin and cardiovascular calcification in hemodialysis patients: a cross-sectional study
Vincent M Brandenburg1, Rafael Kramann, Ralf Koos
1Department of Cardiology, University Hospital of the RWTH, Pauwelsstraße 30, D- 52057 Aachen, Germany. Vincent.Brandenburg@post.rwth-aachen.de.
Insights
Sclerostin is linked to aortic valve calcification in dialysis patients. This protein is locally produced in calcified aortic valves, suggesting a role in the disease process.
Area of Science:
- Nephrology
- Cardiology
- Endocrinology
Background:
- Sclerostin, a Wnt pathway antagonist, influences bone turnover.
- Its role in vascular calcification, particularly in hemodialysis patients, is under investigation.
Purpose of the Study:
- To investigate the association between sclerostin and coronary artery calcification (CAC) and aortic valve calcification (AVC).
- To explore the local expression of sclerostin in calcified aortic valves.
Main Methods:
- Cross-sectional study of 67 chronic hemodialysis (HD) patients using multi-slice computed tomography (MS-CT).
- Serum sclerostin levels measured by ELISA; compared to 54 controls.
- Sclerostin expression analyzed in explanted aortic valves via immunohistochemistry and mRNA quantification.
Main Results:
- CAC and AVC were prevalent in 65% and 40% of HD patients, respectively.
- Serum sclerostin levels were significantly higher in HD patients than controls (p < 0.001).
- Elevated sclerostin levels correlated with AVC (p = 0.02), and local expression was found in calcified aortic valves.
Conclusions:
- Sclerostin is strongly associated with calcifying aortic heart valve disease in hemodialysis patients.
- Sclerostin is locally produced in aortic valve tissue near calcification sites.
Background:
Sclerostin is a Wnt pathway antagonist regulating osteoblast activity and bone turnover. Here, we assessed the potential association of sclerostin with the development of coronary artery (CAC) and aortic valve calcifications (AVC) in haemodialysis (HD) patients.
Methods:
We conducted a cross-sectional multi-slice computed tomography (MS-CT) scanning study in 67 chronic HD patients (59.4 ± 14.8 yrs) for measurement of CAC and AVC. We tested established biomarkers as well as serum sclerostin (ELISA) regarding their association to the presence of calcification. Fifty-four adults without relevant renal disease served as controls for serum sclerostin levels. Additionally, sclerostin expression in explanted aortic valves from 15 dialysis patients was analysed ex vivo by immunohistochemistry and mRNA quantification (Qt-RT-PCR).
Results:
CAC (Agatston score > 100) and any AVC were present in 65% and in 40% of the MS-CT patient group, respectively. Serum sclerostin levels (1.53 ± 0.81 vs 0.76 ± 0.31 ng/mL, p < 0.001) were significantly elevated in HD compared to controls and more so in HD patients with AVC versus those without AVC (1.78 ± 0.84 vs 1.35 ± 0.73 ng/mL, p = 0.02). Multivariable regression analysis for AVC revealed significant associations with higher serum sclerostin. Ex vivo analysis of uraemic calcified aortic valves (n = 10) revealed a strong sclerostin expression very close to calcified regions (no sclerostin staining in non-calcified valves). Correspondingly, we observed a highly significant upregulation of sclerostin mRNA in calcified valves compared to non-calcified control valves.
Conclusion:
We found a strong association of sclerostin with calcifying aortic heart valve disease in haemodialysis patients. Sclerostin is locally produced in aortic valve tissue adjacent to areas of calcification.
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