الفهرس 
IntroductionOnly 14 pages are availabe for public view
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Abstract
Chronic kidney disease patients , whether starting HD or not have 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 implicated in the pathogenesis of vascular calcification, which may promote the cardiovascular events of morbidity and mortality in chronic kidney disease patients, however the role of sclerostin in vascular calcification and clinical prognosis in chronic kidney disease remains elusive.
So we aimed to determine if Sclerostin in chronic Kidney Disease Patients pre dialysis and those on regular hemodialysis has a role in vascular calcification or not. The present Study included 80 CKD patients attending Menoufia University Hospital from July 2018 till January 2019.
The selected patients were compared to 51 control persons of matched age and gender. Patients were classified 40 CKD patients not start HD (group ΙΙ) and 40 CKD patients on regular HD more than six months (group ΙΙΙ) and in comparison with 15 control subjects (group Ι).
Serum Sclerostin level was measured using commercially available enzyme linked immunosorbent assay kits. AAC was assessed using lateral lumbar radiography. Echocardiography was used to assess AVC calcification presence or absence, and we correlated the association between sclerostin levels and vascular calcification.CIMT measured by neck US.
Sclerostin levels among the CKD on HD patients was significantly higher than that of CKD pre-dialysis group which in turn statistically higher than control group .AAC was observed in 16 patients (40 %) in CKD predialysis patients, while in CKD on HD group, 26 patients (65 %) had AAC. AVC was observed in 14 patients (35 %) in CKD predialysis patients, while in CKD on HD group, 21 patients (52.5 %) had AAC. Sclerostin levels were higher in patients with AAC and AVC.
CIMT mean values among the CKD on HD patients were statistically higher than that among the CKD predialysis group which were statistically higher than those among the control group. There was highly significant positive correlation between serum sclerostin level and CIMT.
Using Binary regression analysis, Sclerostin was identified as independent predictor for the presence of AAC & AVC in CKD patients and abnormal CIMT.
Serum Sclerostin at a cut off level ≤ 19.60 can detect the presence of Aortic valve calcification by ECHO with 91% sensitivity and 69% specificity.
Serum Sclerostin at a cut off level ≤ 16.95 can detect the presence of abdominal aortic calcification by X ray with 95% sensitivity and 67% specificity.
Serum Sclerostin at a cut off level ≤17.20 can detect the presence of Abnormal CIMT with 79 % sensitivity and 65% specificity.