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ORIGINAL ARTICLE
Year : 2019  |  Volume : 31  |  Issue : 4  |  Page : 813-821

Study of serum sclerostin levels and its role in vascular calcification in patients with chronic kidney disease


1 Internal Medicine Department, Faculty of Medicine, Menoufia University, Shebeen Elkom, Menoufia, Egypt
2 Clinical Pathology Department, Faculty of Medicine, Menoufia University, Shebeen Elkom, Menoufia, Egypt

Correspondence Address:
MD Amera A Sharaf El Deen
Internal Medicine Department, Faculty of Medicine, Menoufia University, Shebeen Elkom, Menoufia
Egypt
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ejim.ejim_34_19

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Objective The aim of this work was to study serum sclerostin levels in patients with chronic kidney disease (CKD) not on dialysis and those on regular hemodialysis and its role in vascular calcification. Background CKD, whether starting hemodialysis (HD) or not, is associated with an increase in the risk for vascular calcification, which can only be partially explained by known classical risk factors. Sclerostin is an osteocyte-derived inhibitor of the Wnt pathway and has been shown to play a key role in vascular calcification in patients with CKD. Patients and methods This cross-sectional study was carried out on 80 patients with CKD attending Menoufia University Hospital. Patients were classified into 40 patients with CKD who were not on HD (Group II) and 40 patients with CKD on regular HD more than 6 months (Group III), who were compared with 15 controls (Group I). Abdominal aortic calcification (AAC) was assessed using lateral lumbar radiography. Echocardiography was used to assess aortic valve calcification (AVC) calcification. Patient’s basic clinical and biochemical data were recorded. Serum sclerostin level was measured using commercially available enzyme-linked immunosorbent assay kits. Results Sclerostin levels among the patients with CKD on HD (116.8±0.103.69 Pmol/l) was significantly higher than that of CKD predialysis group (28.63±0.36.26 Pmol/l), which in turn was statistically higher than control group (6.6±0.2.9 Pmol) (P=0.000). AAC was observed in 16 (40%) patients in CKD predialysis group, whereas in CKD on HD group, 26 (65%) patients had AAC. AVC was observed in 14 (35%) patients in CKD predialysis group, whereas in CKD on HD group, 21 (52.5%) patients had AVC. Using binary regression analysis, sclerostin was identified as an independent predictor for the presence of AAC (OR: 1.017; P=0.000) and AVC (OR: 1.013; P=0.001) in patients with CKD. Conclusion Patients with CKD (predialysis and on HD) exhibit an increase in sclerostin levels. Sclerostin expansion correlated positively with vascular and valvular calcification. Sclerostin is an independent risk factor for heart valve calcification and AAC in patients with CKD.


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