The Egyptian Journal of Internal Medicine (Jan 2019)

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

  • Ahmed R Elarbagy,
  • Yassein S Yassein,
  • Mahmoud M Emara,
  • Ahmed A Sonbol,
  • Khaled M Zorkaney,
  • Amera A Sharaf El Deen

DOI
https://doi.org/10.4103/ejim.ejim_34_19
Journal volume & issue
Vol. 31, no. 4
pp. 813 – 821

Abstract

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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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