Additional adjustment for available possible mediators (ie, DM, hypertension, eGFR, TGs, and LDL and HDL cholesterol; model 3) led to partial attenuation of the associations between sclerostin and Friesinger score, death from cardiac cause, and coronary artery stenosis, as reflected by 40%, 77%, and 44% decreases in effect estimates respectively (Table 5). This evidence concerns the gene SOST and hypertensive disorder.