Sclerostin Predicts Arterial Calcification in ESRD

The osetocyte-derived bone formation inhibitor sclerostin predicts vascular calcification in patients with end stage renal disease (ESRD), according to a study in Kidney International.

The researchers measured serum sclerostin levels in 89 patients with ESRD, mean age 48 years, who had undergone epigastric artery biopsy. Circulating sclerostin levels were significantly higher in the 37 patients who had moderate to extensive vascular calcification, compared to the 52 with no or minimal calcification. Patients with a coronary artery calcification score of 100 or higher also had higher sclerostin levels: 559 versus 367 pg/mL, respectively.

Serum sclerostin was correlated with patient age, intact parathyroid hormone and bone-specific alkaline phosphatase levels, and percent calcification. On multivariate analysis, sclerostin, age, and male sex were all independently associated with medical vascular calcification.

On receiver operating characteristic curve analysis, sclerostin was a significant predictor of vascular calcification, with an area under the curve of 0.68. There was little or no expression of vascular sclerostin mRNA and protein, suggesting that vascular-derived sclerostin in not a major contributor to circulating levels.

Recent evidence suggests that sclerostin may be an important contributor to vascular calcification and bone disorders associated with chronic kidney disease–mineral and bone disorder (CKD-MBD). The new results show that high serum sclerostin levels are associated with several measures of increased vascular calcification in ESRD patients.

Of several circulating CKD-MBD biomarkers evaluated, sclerostin is the only one that predicts vascular calcification. The authors discuss the implications for understanding the development of arterial calcification in kidney disease [Qureshi AR, et al. Increased circulating sclerostin levels in end stage renal disease predict biopsy-verified vascular medial calcification and coronary artery calcification. Kidney Int 2015; 88:1356–1364].