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. Here, PTH is linked to chronic kidney disease.