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NDT Plus 2008 1(Supplement 1):i2-i6; doi:10.1093/ndtplus/sfm037
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© The Author [2007].
The online version of this article has been published under an open access model. Users are entitled to use, reproduce, disseminate, or display the open access version of this article for non-commercial purposes provided that: the original authorship is properly and fully attributed; the Journal and Oxford University Press are attributed as the original place of publication with the correct citation details given; if an article is subsequently reproduced or disseminated not in its entirety but only in part or as a derivative work this must be clearly indicated. For commercial re-use, please contact journals.permissions@oxfordjournals.org

The Pathophysiology of Secondary Hyperparathyroidism and the Consequences of Uncontrolled Mineral Metabolism in Chronic Kidney Disease: The Role of COSMOS

Jorge B. Cannata-Andía1 and Fernando Carrera2

1 University of Oviedo, Oviedo, Spain
2 Eurodial, Euromedic, Dialysis Unit, Leiria, Portugal

Correspondence: Jorge B. Cannata-Andía, Universidad de Oviedo, Servicio de Metabolismo Oseo y Mineral, Instituto Reina Sofia de Investigacion, Hospital Central de Asturias, C/Julian Claveria s/n, Oviedo, Spain E33006. E-mail: cannata{at}hca.es


  Abstract

The development of secondary hyperparathyroidism (SHPT) is a common complication of chronic kidney disease. SHPT develops as a consequence of mineral metabolism disturbances and is characterized by elevated serum parathyroid hormone (PTH) and parathyroid hyperplasia. Evidence suggests that SHPT contributes to the development of vascular calcification and cardiovascular disease, as well as to the development of renal osteodystrophy. The elevated serum calcium, phosphorus, calcium–phosphorus product and PTH that accompany SHPT have been independently associated with an increased relative risk of mortality. Despite the danger that these risks represent, achieving control of mineral metabolism in SHPT is difficult. Recent evidence from the Current Management of Secondary Hyperparathyroidism: Multicentre Observational Study has shown that fewer than 1 in 10 haemodialysis patients simultaneously meet their National Kidney Foundation Kidney Disease Outcomes Quality Initiative targets for serum calcium, phosphorus, calcium–phosphorus product and PTH with standard treatments. There is therefore an urgent need for new strategies and novel pharmacologic therapies that improve control of mineral metabolism and PTH secretion in SHPT and thus reduce the mortality associated with this condition.

Key Words: calcium • haemodialysis • kidney • phosphorus • secondary hyperparathyroidism

Received for publication July 17, 2007. Accepted for publication September 10, 2007.


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