Wei Lv1, Lina Guan2, Yan Zhang3, Shengqiang Yu4, Bofeng Cao5, Yongqiang Ji1. 1. Department of Nephrology, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, 264000, Shandong, China. 2. Neurological Intensive Care Unit, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, 264000, Shandong, China. 3. Department of Nephrology, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, 264000, Shandong, China. cnwdoc@126.com. 4. Department of Urology, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, 264000, Shandong, China. 5. Medical Imaging Center, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, 264000, Shandong, China.
Abstract
BACKGROUND: Sclerostin is an osteocyte-derived inhibitor of the Wnt pathway and has been shown to play a key role in chronic kidney disease-mineral and bone disorder (CKD-MBD). The present study aimed to validate its potential as a predictor of vascular calcification in patients with CKD stages 3-4. METHODS: A total of 97 patients with CKD stages 3-4 were enrolled in this cross-sectional study. Routine clinical biochemistry tests and assays for sclerostin and mineral metabolism markers were performed. Additionally, vascular calcification was assessed by multislice spiral computed tomography. Logistic regression analyses were used to study the relationships between sclerostin and vascular calcification. RESULTS: Serum sclerostin levels (30.8 ± 6.4 vs. 41.7 ± 12.6 pmol/L, P < 0.05) were significantly elevated in patients with CKD stage 3a compared to in controls and increased with the decline in glomerular filtration rates. Furthermore, patients with vascular calcification had higher serum sclerostin levels. Patients with sclerostin levels above the median value had increased the prevalence of vascular calcification. Multivariate analysis revealed that sclerostin levels were positively associated with vascular calcification. CONCLUSION: Our data indicate that sclerostin levels are elevated in patients with CKD and are associated with vascular calcification. Therefore, sclerostin may be used as a predictor of vascular calcification in the clinical setting.
BACKGROUND:Sclerostin is an osteocyte-derived inhibitor of the Wnt pathway and has been shown to play a key role in chronic kidney disease-mineral and bone disorder (CKD-MBD). The present study aimed to validate its potential as a predictor of vascular calcification in patients with CKD stages 3-4. METHODS: A total of 97 patients with CKD stages 3-4 were enrolled in this cross-sectional study. Routine clinical biochemistry tests and assays for sclerostin and mineral metabolism markers were performed. Additionally, vascular calcification was assessed by multislice spiral computed tomography. Logistic regression analyses were used to study the relationships between sclerostin and vascular calcification. RESULTS: Serum sclerostin levels (30.8 ± 6.4 vs. 41.7 ± 12.6 pmol/L, P < 0.05) were significantly elevated in patients with CKD stage 3a compared to in controls and increased with the decline in glomerular filtration rates. Furthermore, patients with vascular calcification had higher serum sclerostin levels. Patients with sclerostin levels above the median value had increased the prevalence of vascular calcification. Multivariate analysis revealed that sclerostin levels were positively associated with vascular calcification. CONCLUSION: Our data indicate that sclerostin levels are elevated in patients with CKD and are associated with vascular calcification. Therefore, sclerostin may be used as a predictor of vascular calcification in the clinical setting.
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