Abstract
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 × P) is a consistent feature of calcimimetic therapy and may facilitate the achievement of SHPT treatment targets. © ERA-EDTA 2004; all rights reserved.
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Cunningham, J. (2004). Achieving therapeutic targets in the treatment of secondary hyperparathyroidism. Nephrology Dialysis Transplantation, 19(SUPPL. 5). https://doi.org/10.1093/ndt/gfh1050
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