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Vitamin D and kidney disease
Calcium and phosphorus are essential minerals required for many critical biologic functions including cell signaling, energy metabolism, skeletal growth and integrity. Calcium and phosphate homeostasis are maintained primarily by regulation of epithelial calcium and phosphate cotransport in the kidn...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Elsevier
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6303542/ https://www.ncbi.nlm.nih.gov/pubmed/30591927 http://dx.doi.org/10.1016/j.bonr.2018.07.002 |
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author | Keung, Lisa Perwad, Farzana |
author_facet | Keung, Lisa Perwad, Farzana |
author_sort | Keung, Lisa |
collection | PubMed |
description | Calcium and phosphorus are essential minerals required for many critical biologic functions including cell signaling, energy metabolism, skeletal growth and integrity. Calcium and phosphate homeostasis are maintained primarily by regulation of epithelial calcium and phosphate cotransport in the kidney and intestine, processes that are tightly regulated by hormones including 1,25 dihydroxyvitamin D (1,25(OH)(2)D), fibroblast growth factor 23 (FGF23) and parathyroid hormone (PTH). In patients with chronic kidney disease (CKD), as renal function declines, disruption of feedback loops between these hormones have adverse consequences on several organ systems, including the skeleton, heart and vascular system. CKD-associated mineral and bone disorder (CKD-MBD) is defined as a systemic disorder of mineral and bone metabolism due to CKD manifested by abnormalities of calcium, phosphorus, PTH or vitamin D metabolism, abnormalities of bone turnover, mineralization and volume, and ectopic soft tissue calcification. Complications of CKD-MBD include vascular calcification, stroke, skeletal fracture and increased risk of death. Increased FGF23 and PTH concentrations, and 1,25(OH)(2)D deficiency contribute to the pathogenesis of CKD-MBD. Therefore, treatment of patients with CKD-MBD is focused on restoring the feedback loops to maintain normal calcium and phosphate balance to prevent skeletal and cardiovascular complications. |
format | Online Article Text |
id | pubmed-6303542 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Elsevier |
record_format | MEDLINE/PubMed |
spelling | pubmed-63035422018-12-27 Vitamin D and kidney disease Keung, Lisa Perwad, Farzana Bone Rep Articles from the Special Issue on Bone Health-Vitamin D; Edited by Prof Daniel Bikle and Prof Roger Bouillon Calcium and phosphorus are essential minerals required for many critical biologic functions including cell signaling, energy metabolism, skeletal growth and integrity. Calcium and phosphate homeostasis are maintained primarily by regulation of epithelial calcium and phosphate cotransport in the kidney and intestine, processes that are tightly regulated by hormones including 1,25 dihydroxyvitamin D (1,25(OH)(2)D), fibroblast growth factor 23 (FGF23) and parathyroid hormone (PTH). In patients with chronic kidney disease (CKD), as renal function declines, disruption of feedback loops between these hormones have adverse consequences on several organ systems, including the skeleton, heart and vascular system. CKD-associated mineral and bone disorder (CKD-MBD) is defined as a systemic disorder of mineral and bone metabolism due to CKD manifested by abnormalities of calcium, phosphorus, PTH or vitamin D metabolism, abnormalities of bone turnover, mineralization and volume, and ectopic soft tissue calcification. Complications of CKD-MBD include vascular calcification, stroke, skeletal fracture and increased risk of death. Increased FGF23 and PTH concentrations, and 1,25(OH)(2)D deficiency contribute to the pathogenesis of CKD-MBD. Therefore, treatment of patients with CKD-MBD is focused on restoring the feedback loops to maintain normal calcium and phosphate balance to prevent skeletal and cardiovascular complications. Elsevier 2018-07-25 /pmc/articles/PMC6303542/ /pubmed/30591927 http://dx.doi.org/10.1016/j.bonr.2018.07.002 Text en © 2018 The Authors http://creativecommons.org/licenses/by-nc-nd/4.0/ This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/). |
spellingShingle | Articles from the Special Issue on Bone Health-Vitamin D; Edited by Prof Daniel Bikle and Prof Roger Bouillon Keung, Lisa Perwad, Farzana Vitamin D and kidney disease |
title | Vitamin D and kidney disease |
title_full | Vitamin D and kidney disease |
title_fullStr | Vitamin D and kidney disease |
title_full_unstemmed | Vitamin D and kidney disease |
title_short | Vitamin D and kidney disease |
title_sort | vitamin d and kidney disease |
topic | Articles from the Special Issue on Bone Health-Vitamin D; Edited by Prof Daniel Bikle and Prof Roger Bouillon |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6303542/ https://www.ncbi.nlm.nih.gov/pubmed/30591927 http://dx.doi.org/10.1016/j.bonr.2018.07.002 |
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