Serum sclerostin as a potential novel biomarker for heart valve calcification in patients with chronic kidney disease

Y.-Q. Ji, L.-N. Guan, S.-X. Yu, P.-Y. Yin, X.-Q. Shen, Z.-W. Sun, J. Liu, W. Lv, G.-P. Yu, C. Ren

Department of Nephrology, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, Shandong Province, China. renchaorc@hotmail.com

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• Nephrology

OBJECTIVE: To explore the correlation between change in sclerostin level and heart valve calcification in patients with chronic kidney disease (CKD) in stages 3-5, as well as the possible underlying mechanism, which could provide a clinical reference for the diagnosis and treatment of cardiovascular disease (CVD).

PATIENTS AND METHODS: 110 patients were divided into a healthy control group and three groups of patients with CKD stages 3, 4, and 5 according to CKD staging guidelines. Scr, BUN, AKP, TC, TG, HDL, LDL, Ca, Pi, and CRP were measured, and calcium-phosphate product (Ca×Pi) calculated. ELISA was used to measure the sclerostin level, and the estimated glomerular filtration rate (eGFR) was calculated by MDRD. Heart valve calcification was measured by a physician in the Cardiac Department of our hospital. The correlations between sclerostin-level change and heart valve calcification, as well as each index in CKD patients in stages 3–5, were analyzed.

RESULTS: Compared with the healthy control group, the serum Ca in CKD stage-3, stage-4, and stage-5 groups (p < 0.05) was reduced, and PTH was increased (p < 0.05). Blood Pi and Ca×Pi in the stage-4 and stage-5 groups were increased (p < 0.05). The serum sclerostin level increased with renal hypofunction in stage-3 CKD patients, and was significantly increased compared with that of the control group, reaching the highest level in the terminal stage (p < 0.01). Pearson correlation analysis indicated that serum sclerostin was negatively correlated with eGFR (r = −0.91, p < 0.001) and blood Ca (r= −0.271, p < 0.001), and positively correlated with SCr (r = 0.608, p < 0.001), blood Pi level (r = 0.295, p < 0.001), PTH (r = 0.334, p < 0.001), and Ca×Pi (r = 0.275, p < 0.001). The rate of heart valve calcification in the CKD patients in stage 5 was relatively high (11/30, 36.67%), and significantly higher than that in healthy controls (1/20, 5%; p < 0.01). Logistic regression analysis of heart valve calcification indicated that sclerostin was a risk factor for heart valve calcification in CKD patients in stages 3–5.

CONCLUSIONS: The sclerostin level gradually increased with renal hypofunction in CKD patients in stages 3–5, and the increase in serum sclerostin level in the CKD patients occurred earlier than the change in Pi and Ca×Pi. The risk of heart valve calcification in stage-5 CKD patients was significantly increased. Sclerostin is an independent risk factor for heart valve calcification in CKD patients.

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