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 language | English (US) |
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Title of host publication | Chronic Renal Disease |
Publisher | Elsevier |
Pages | 661-679 |
Number of pages | 19 |
ISBN (Electronic) | 9780128158760 |
ISBN (Print) | 9780128158777 |
DOIs | |
State | Published - Jan 1 2019 |
Keywords
- Bone
- Calcium
- Cardiovascular disease
- CKD-MBD
- Hormones
- Magnesium
- Phosphate
- Pi binding
- Vascular calcification
ASJC Scopus subject areas
- General Agricultural and Biological Sciences
- General Biochemistry, Genetics and Molecular Biology