SOST and secondary hyperparathyroidism: In vivo Sost−/− mice were detected with the phenotype in the setting of chronic renal failure with severe secondary hyperparathyroidism, in addition to the high bone mass phenotype of Sost deficiency.249 In another study with juvenile cystic kidney (JCK) mouse, a model of polycystic kidney disease (PKD) that carries a mutation of the Nek8 serine-threonine kinase, increased expression of Wnt antagonists (sclerostin and sFRP4) were reported.250 These data suggest that the circulating level of sclerostin is associated with kidney function.