SOST and secondary hyperparathyroidism: Current data suggest that increasing PTH levels suppress osteocytic sclerostin expression;[12] however, bone sclerostin is increased in CKD.[7] Circulating phosphorus and PTH both increase FGF23 concentrations[13, 14] and therapies used to treat renal osteodystrophy, in addition to controlling secondary hyperparathyroidism and bone turnover, likely also alter osteocytic protein expression, potentially via changes in mineral metabolism.