Achieving therapeutic targets in the treatment of secondary hyperparathyroidism.

Disturbances in the control of extracellular ionized calcium and phosphorus concentrations, and vitamin D metabolism, in patients with chronic kidney disease (CKD) are associated with prolonged stimulation of the parathyroid glands. This results in increased synthesis and release of parathyroid hormone (PTH) and parathyroid hyperplasia-secondary hyperparathyroidism (SHPT). SHPT is in turn a major driver of the skeletal disturbance that characterizes renal osteodystrophy and is associated with vascular and other soft tissue calcification. Current therapeutic strategies based on vitamin D compounds and calcium-containing phosphate binders are difficult to implement effectively because both agents are associated with substantial, and often dose-limiting, calcaemic actions that prevent the attainment of treatment targets. Calcimimetics are novel agents that increase the sensitivity of calcium-sensing receptors in the parathyroid glands. Consequently, they allow simultaneous reduction of both PTH and extracellular calcium concentrations, thus differing from currently available vitamin D therapies. Reduction of the calcium-phosphorus product (Ca x P) is a consistent feature of calcimimetic therapy and may facilitate the achievement of SHPT treatment targets.