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Nephrol Dial Transplant (2004) 19: v9-v14
Nephrol Dial Transplant Vol. 19 Suppl 5 © ERA–EDTA 2004; all rights reserved

Achieving therapeutic targets in the treatment of secondary hyperparathyroidism

John Cunningham

Department of Nephrology, The Middlesex Hospital, London, UK

Correspondence and offprint requests to: Professor John Cunningham, Department of Nephrology, The Middlesex Hospital, University College London Hospitals, Mortimer Street, London W1T 3AA, UK. Email: john.cunningham{at}uclh.org

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 x P) is a consistent feature of calcimimetic therapy and may facilitate the achievement of SHPT treatment targets.

Keywords: calcimimetic therapy; calcium x phosphorus; chronic kidney disease; parathyroid hormone; secondary hyperparathyroidism


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Nephrol. Dial. Transplant., October 1, 2006; 21(10): 2989 - 2990.
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