Calcium regulation and bone mineral metabolism in elderly patients with chronic kidney disease

Vickram Tejwani, Qi Qian

Research output: Contribution to journalReview article

19 Scopus citations


The elderly chronic kidney disease (CKD) population is growing. Both aging and CKD can disrupt calcium (Ca2+) homeostasis and cause alterations of multiple Ca2+-regulatory mechanisms, including parathyroid hormone, vitamin D, fibroblast growth factor-23/Klotho, calcium-sensing receptor and Ca2+-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 Ca2+ 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.

Original languageEnglish (US)
Pages (from-to)1913-1936
Number of pages24
Issue number6
StatePublished - May 29 2013



  • Aging
  • Calcium homeostasis
  • Chronic kidney disease
  • Mineral and bone disorder
  • Secondary hyperparathyroidism
  • Vascular calcification

ASJC Scopus subject areas

  • Food Science
  • Nutrition and Dietetics

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