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

Nutrients. 2013 May 29;5(6):1913-36. doi: 10.3390/nu5061913.

Abstract

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.

Publication types

  • Review

MeSH terms

  • Aged
  • Aging / physiology*
  • Animals
  • Bone Density / physiology*
  • Bone Diseases, Metabolic / complications
  • Bone Diseases, Metabolic / physiopathology*
  • Bone Diseases, Metabolic / therapy
  • Calcium / metabolism*
  • Female
  • Fibroblast Growth Factor-23
  • Fibroblast Growth Factors / blood
  • Fibroblast Growth Factors / deficiency
  • Glucuronidase / blood
  • Glucuronidase / deficiency
  • Guidelines as Topic
  • Homeostasis
  • Humans
  • Klotho Proteins
  • Male
  • Parathyroid Hormone / blood
  • Phosphates / blood
  • Receptors, Calcium-Sensing / blood
  • Renal Insufficiency, Chronic / complications
  • Renal Insufficiency, Chronic / physiopathology*
  • Renal Insufficiency, Chronic / therapy
  • Vitamin D / blood

Substances

  • Parathyroid Hormone
  • Phosphates
  • Receptors, Calcium-Sensing
  • Vitamin D
  • Fibroblast Growth Factors
  • Fibroblast Growth Factor-23
  • Glucuronidase
  • Klotho Proteins
  • Calcium