This pattern strongly indicates that declining renal function is associated with increased circulating sclerostin, likely due to impaired renal clearance of sclerostin, increased production of sclerostin by osteocytes in response to renal injury as a compensatory or self-defense mechanism, interaction with other chronic kidney disease biomarkers (such as fibroblast growth factor-23), and activation of the Wnt/β-catenin signaling or activin (transforming growth factor-β family) [38,39,40,41,42]. Here, INHBE is linked to chronic kidney disease.