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Calcium Regulation and Bone Mineral Metabolism in Elderly Patients with Chronic Kidney Disease

The elderly chronic kidney disease (CKD) population is growing. Both aging and CKD can disrupt calcium (Ca(2+)) homeostasis and cause alterations of multiple Ca(2+)-regulatory mechanisms, including parathyroid hormone, vitamin D, fibroblast growth factor-23/Klotho, calcium-sensing receptor and Ca(2+...

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Detalles Bibliográficos
Autores principales: Tejwani, Vickram, Qian, Qi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3725483/
https://www.ncbi.nlm.nih.gov/pubmed/23760058
http://dx.doi.org/10.3390/nu5061913
Descripción
Sumario:The elderly chronic kidney disease (CKD) population is growing. Both aging and CKD can disrupt calcium (Ca(2+)) homeostasis and cause alterations of multiple Ca(2+)-regulatory mechanisms, including parathyroid hormone, vitamin D, fibroblast growth factor-23/Klotho, calcium-sensing receptor and Ca(2+)-phosphate product. These alterations can be deleterious to bone mineral metabolism and soft tissue health, leading to metabolic bone disease and vascular calcification and aging, termed CKD-mineral and bone disorder (MBD). CKD-MBD is associated with morbid clinical outcomes, including fracture, cardiovascular events and all-cause mortality. In this paper, we comprehensively review Ca(2+) regulation and bone mineral metabolism, with a special emphasis on elderly CKD patients. We also present the current treatment-guidelines and management options for CKD-MBD.