Vascular calcification and increased mortality is now well linked in hemodialysis (HD) patients. Among the inhibitors and promoters of calcium-phosphate and bone metabolism, we studied Sclerostin, a glycoprotein mainly expressed by osteocytes, involved in regulating bone formation by inhibiting Wnt–β-catenin signaling. Studies demonstrated, in experimental CDK animal model, a positive association between Sclerostin production and dietary phosphate intake.

Materials and Methods

We investigated the relation between Sclerostin levels (SL) and dietary habits in 49 Caucasian HD patients (age 36–90, M/F 31/18, dialysis vintage 1–144 months). Nutrient intake was analyzed with 24 h-recall method. Serum Sclerostin was measured by ELISA method. Statistically analysis was performed by SPSS software.


Mean calcium and phosphate intake were 705 ± 584 and 1196 ± 498 mg/day, respectively. Serum SL (3356 ± 2118 pg/ml) were increased in HD patients. Positive correlation was found between serum SL and calcium (r = 0.33, p = 0.025) and phosphate intake (r = 0.34, p = 0.021). Patients with SL higher were older (p = 0.003), showed higher protein (p = 0.012), calcium (p = 0.017) and phosphate (p = 0.004) intake. Multiple linear regression testing Sclerostin as dependent variable (dialysis vintage, age, body-weight, serum calcium and phosphate, serum PTH, calcium and phosphate intake as independent variables) found that dietary phosphate intake was the only significant determinant of SL (r = 0.356, B = 1.5, p = 0.004). In Patients with calcium carbonate or acetate therapy (n = 31), serum SL was positively correlated with dietary calcium (r = 0.433, p = 0.017) and phosphate intake (r = 0.377, p = 0.04).


The dietary phosphate and calcium intake may influence serum Sclerostin levels and potentially affect bone remodeling or soft tissue calcification in HD patients.


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