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.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 1913-1936 |
| Number of pages | 24 |
| Journal | Nutrients |
| Volume | 5 |
| Issue number | 6 |
| DOIs | |
| State | Published - May 29 2013 |
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Keywords
- Aging
- Calcium homeostasis
- Chronic kidney disease
- Mineral and bone disorder
- Secondary hyperparathyroidism
- Vascular calcification
ASJC Scopus subject areas
- Food Science
- Nutrition and Dietetics
Cite this
Calcium regulation and bone mineral metabolism in elderly patients with chronic kidney disease. / Tejwani, Vickram; Qian, Qi.
In: Nutrients, Vol. 5, No. 6, 29.05.2013, p. 1913-1936.Research output: Contribution to journal › Review article
}
TY - JOUR
T1 - Calcium regulation and bone mineral metabolism in elderly patients with chronic kidney disease
AU - Tejwani, Vickram
AU - Qian, Qi
PY - 2013/5/29
Y1 - 2013/5/29
N2 - 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.
AB - 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.
KW - Aging
KW - Calcium homeostasis
KW - Chronic kidney disease
KW - Mineral and bone disorder
KW - Secondary hyperparathyroidism
KW - Vascular calcification
UR - http://www.scopus.com/inward/record.url?scp=84878431459&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84878431459&partnerID=8YFLogxK
U2 - 10.3390/nu5061913
DO - 10.3390/nu5061913
M3 - Review article
VL - 5
SP - 1913
EP - 1936
JO - Nutrients
JF - Nutrients
SN - 2072-6643
IS - 6
ER -