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Vascular Calcification and Renal Bone Disorders
At the early stage of chronic kidney disease (CKD), the systemic mineral metabolism and bone composition start to change. This alteration is known as chronic kidney disease-mineral bone disorder (CKD-MBD). It is well known that the bone turnover disorder is the most common complication of CKD-MBD. B...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi Publishing Corporation
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4127293/ https://www.ncbi.nlm.nih.gov/pubmed/25136676 http://dx.doi.org/10.1155/2014/637065 |
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author | Lu, Kuo-Cheng Wu, Chia-Chao Yen, Jen-Fen Liu, Wen-Chih |
author_facet | Lu, Kuo-Cheng Wu, Chia-Chao Yen, Jen-Fen Liu, Wen-Chih |
author_sort | Lu, Kuo-Cheng |
collection | PubMed |
description | At the early stage of chronic kidney disease (CKD), the systemic mineral metabolism and bone composition start to change. This alteration is known as chronic kidney disease-mineral bone disorder (CKD-MBD). It is well known that the bone turnover disorder is the most common complication of CKD-MBD. Besides, CKD patients usually suffer from vascular calcification (VC), which is highly associated with mortality. Many factors regulate the VC mechanism, which include imbalances in serum calcium and phosphate, systemic inflammation, RANK/RANKL/OPG triad, aldosterone, microRNAs, osteogenic transdifferentiation, and effects of vitamins. These factors have roles in both promoting and inhibiting VC. Patients with CKD usually have bone turnover problems. Patients with high bone turnover have increase of calcium and phosphate release from the bone. By contrast, when bone turnover is low, serum calcium and phosphate levels are frequently maintained at high levels because the reservoir functions of bone decrease. Both of these conditions will increase the possibility of VC. In addition, the calcified vessel may secrete FGF23 and Wnt inhibitors such as sclerostin, DKK-1, and secreted frizzled-related protein to prevent further VC. However, all of them may fight back the inhibition of bone formation resulting in fragile bone. There are several ways to treat VC depending on the bone turnover status of the individual. The main goals of therapy are to maintain normal bone turnover and protect against VC. |
format | Online Article Text |
id | pubmed-4127293 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | Hindawi Publishing Corporation |
record_format | MEDLINE/PubMed |
spelling | pubmed-41272932014-08-18 Vascular Calcification and Renal Bone Disorders Lu, Kuo-Cheng Wu, Chia-Chao Yen, Jen-Fen Liu, Wen-Chih ScientificWorldJournal Review Article At the early stage of chronic kidney disease (CKD), the systemic mineral metabolism and bone composition start to change. This alteration is known as chronic kidney disease-mineral bone disorder (CKD-MBD). It is well known that the bone turnover disorder is the most common complication of CKD-MBD. Besides, CKD patients usually suffer from vascular calcification (VC), which is highly associated with mortality. Many factors regulate the VC mechanism, which include imbalances in serum calcium and phosphate, systemic inflammation, RANK/RANKL/OPG triad, aldosterone, microRNAs, osteogenic transdifferentiation, and effects of vitamins. These factors have roles in both promoting and inhibiting VC. Patients with CKD usually have bone turnover problems. Patients with high bone turnover have increase of calcium and phosphate release from the bone. By contrast, when bone turnover is low, serum calcium and phosphate levels are frequently maintained at high levels because the reservoir functions of bone decrease. Both of these conditions will increase the possibility of VC. In addition, the calcified vessel may secrete FGF23 and Wnt inhibitors such as sclerostin, DKK-1, and secreted frizzled-related protein to prevent further VC. However, all of them may fight back the inhibition of bone formation resulting in fragile bone. There are several ways to treat VC depending on the bone turnover status of the individual. The main goals of therapy are to maintain normal bone turnover and protect against VC. Hindawi Publishing Corporation 2014 2014-07-17 /pmc/articles/PMC4127293/ /pubmed/25136676 http://dx.doi.org/10.1155/2014/637065 Text en Copyright © 2014 Kuo-Cheng Lu et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Review Article Lu, Kuo-Cheng Wu, Chia-Chao Yen, Jen-Fen Liu, Wen-Chih Vascular Calcification and Renal Bone Disorders |
title | Vascular Calcification and Renal Bone Disorders |
title_full | Vascular Calcification and Renal Bone Disorders |
title_fullStr | Vascular Calcification and Renal Bone Disorders |
title_full_unstemmed | Vascular Calcification and Renal Bone Disorders |
title_short | Vascular Calcification and Renal Bone Disorders |
title_sort | vascular calcification and renal bone disorders |
topic | Review Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4127293/ https://www.ncbi.nlm.nih.gov/pubmed/25136676 http://dx.doi.org/10.1155/2014/637065 |
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