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

Vickram Tejwani; Qi Qian

doi:10.3390/nu5061913

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

Vickram Tejwani
, Qi Qian

Nephrology and Hypertension

Research output: Contribution to journal › Review article › peer-review

20 Scopus citations

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	https://doi.org/10.3390/nu5061913
State	Published - May 29 2013

Keywords

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

ASJC Scopus subject areas

Food Science
Nutrition and Dietetics

Access to Document

10.3390/nu5061913

Cite this

@article{6b75af77944b4de39ffff4208511eeaf,

title = "Calcium regulation and bone mineral metabolism in elderly patients with chronic kidney disease",

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.",

keywords = "Aging, Calcium homeostasis, Chronic kidney disease, Mineral and bone disorder, Secondary hyperparathyroidism, Vascular calcification",

author = "Vickram Tejwani and Qi Qian",

year = "2013",

month = may,

day = "29",

doi = "10.3390/nu5061913",

language = "English (US)",

volume = "5",

pages = "1913--1936",

journal = "Nutrients",

issn = "2072-6643",

publisher = "Multidisciplinary Digital Publishing Institute (MDPI)",

number = "6",

}

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 - https://www.scopus.com/pages/publications/84878431459

UR - https://www.scopus.com/pages/publications/84878431459#tab=citedBy

U2 - 10.3390/nu5061913

DO - 10.3390/nu5061913

M3 - Review article

C2 - 23760058

AN - SCOPUS:84878431459

SN - 2072-6643

VL - 5

SP - 1913

EP - 1936

JO - Nutrients

JF - Nutrients

IS - 6

ER -

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

Abstract

Keywords

ASJC Scopus subject areas

Access to Document

Other files and links

Fingerprint

Cite this