Calcium, Phosphate, and Magnesium Metabolism in Chronic Kidney Disease

Silvia Ferrè, Javier A. Neyra, Orson W. Moe

Research output: Chapter in Book/Report/Conference proceedingChapter

3 Scopus citations

Abstract

Disturbances in calcium (Ca2+), phosphate (Pi), and magnesium (Mg2+) homeostasis contribute to Chronic Kidney Disease Mineral and Bone Disorders (CKD-MBD), which encompasses abnormalities in mineral metabolism and bone, extraskeletal calcification, and cardiovascular disease. Although the role of excess Pi is unequivocal in CKD-MBD, the role of Ca2+ and Mg2+ is less clear. Understanding how Ca2+, Pi, and Mg2+ disturbances affect the onset and progression of CKD-MBD is essential to achieving the ultimate goal of developing individualized effective treatments that target different facets of CKD-MBD pathophysiology in each patient. Pi load to the organism can be reduced by dietary modifications, binders, and/or modifiers of intestinal epithelial transport. Ca2+ and/or Mg2+ supplements (or avoidance) should be prescribed only to those who will benefit based on Ca2+ and Mg2+ status. Multiple therapies targeting more than one pathophysiologic factor involved in Ca2+, Pi, and Mg2+ balance will be required to treat CKD-MBD.

Original languageEnglish (US)
Title of host publicationChronic Renal Disease
PublisherElsevier
Pages661-679
Number of pages19
ISBN (Electronic)9780128158760
ISBN (Print)9780128158777
DOIs
StatePublished - Jan 1 2019
Externally publishedYes

Keywords

  • Bone
  • Calcium
  • Cardiovascular disease
  • CKD-MBD
  • Hormones
  • Magnesium
  • Phosphate
  • Pi binding
  • Vascular calcification

ASJC Scopus subject areas

  • Agricultural and Biological Sciences(all)
  • Biochemistry, Genetics and Molecular Biology(all)

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