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Bone mineral density and mortality in end-stage renal disease patients
Osteoporosis characterized by low bone mineral density (BMD) as assessed by dual-energy X-ray absorptiometry (DXA) is common among end-stage renal disease (ESRD) patients and associates with high fracture incidence and high all-cause mortality. This is because chronic kidney disease-mineral bone dis...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Oxford University Press
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7367137/ https://www.ncbi.nlm.nih.gov/pubmed/32699616 http://dx.doi.org/10.1093/ckj/sfaa089 |
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author | Iseri, Ken Dai, Lu Chen, Zhimin Qureshi, Abdul Rashid Brismar, Torkel B Stenvinkel, Peter Lindholm, Bengt |
author_facet | Iseri, Ken Dai, Lu Chen, Zhimin Qureshi, Abdul Rashid Brismar, Torkel B Stenvinkel, Peter Lindholm, Bengt |
author_sort | Iseri, Ken |
collection | PubMed |
description | Osteoporosis characterized by low bone mineral density (BMD) as assessed by dual-energy X-ray absorptiometry (DXA) is common among end-stage renal disease (ESRD) patients and associates with high fracture incidence and high all-cause mortality. This is because chronic kidney disease-mineral bone disorders (CKD-MBDs) promote not only bone disease (osteoporosis and renal dystrophy) but also vascular calcification and cardiovascular disease. The disturbed bone metabolism in ESRD leads to ‘loss of cortical bone’ with increased cortical porosity and thinning of cortical bone rather than to loss of trabecular bone. Low BMD, especially at cortical-rich bone sites, is closely linked to CKD-MBD, vascular calcification and poor cardiovascular outcomes. These effects appear to be largely mediated by shared mechanistic pathways via the ‘bone–vascular axis’ through which impaired bone status associates with changes in the vascular wall. Thus, bone is more than just the scaffolding that holds the body together and protects organs from external forces but is—in addition to its physical supportive function—also an active endocrine organ that interacts with the vasculature by paracrine and endocrine factors through pathways including Wnt signalling, osteoprotegerin (OPG)/receptor activator of nuclear factor-κB (RANK)/RANK ligand system and the Galectin-3/receptor of advanced glycation end products axis. The insight that osteogenesis and vascular calcification share many similarities—and the knowledge that vascular calcification is a cell-mediated active rather than a passive mineralization process—suggest that low BMD and vascular calcification (‘vascular ossification’) to a large extent represent two sides of the same coin. Here, we briefly review changes of BMD in ESRD as observed using different DXA methods (central and whole-body DXA) at different bone sites for BMD measurements, and summarize recent knowledge regarding the relationships between ‘low BMD’ and ‘fracture incidence, vascular calcification and increased mortality’ in ESRD patients, as well as potential ‘molecular mechanisms’ underlying these associations. |
format | Online Article Text |
id | pubmed-7367137 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Oxford University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-73671372020-07-21 Bone mineral density and mortality in end-stage renal disease patients Iseri, Ken Dai, Lu Chen, Zhimin Qureshi, Abdul Rashid Brismar, Torkel B Stenvinkel, Peter Lindholm, Bengt Clin Kidney J CKJ Reviews Osteoporosis characterized by low bone mineral density (BMD) as assessed by dual-energy X-ray absorptiometry (DXA) is common among end-stage renal disease (ESRD) patients and associates with high fracture incidence and high all-cause mortality. This is because chronic kidney disease-mineral bone disorders (CKD-MBDs) promote not only bone disease (osteoporosis and renal dystrophy) but also vascular calcification and cardiovascular disease. The disturbed bone metabolism in ESRD leads to ‘loss of cortical bone’ with increased cortical porosity and thinning of cortical bone rather than to loss of trabecular bone. Low BMD, especially at cortical-rich bone sites, is closely linked to CKD-MBD, vascular calcification and poor cardiovascular outcomes. These effects appear to be largely mediated by shared mechanistic pathways via the ‘bone–vascular axis’ through which impaired bone status associates with changes in the vascular wall. Thus, bone is more than just the scaffolding that holds the body together and protects organs from external forces but is—in addition to its physical supportive function—also an active endocrine organ that interacts with the vasculature by paracrine and endocrine factors through pathways including Wnt signalling, osteoprotegerin (OPG)/receptor activator of nuclear factor-κB (RANK)/RANK ligand system and the Galectin-3/receptor of advanced glycation end products axis. The insight that osteogenesis and vascular calcification share many similarities—and the knowledge that vascular calcification is a cell-mediated active rather than a passive mineralization process—suggest that low BMD and vascular calcification (‘vascular ossification’) to a large extent represent two sides of the same coin. Here, we briefly review changes of BMD in ESRD as observed using different DXA methods (central and whole-body DXA) at different bone sites for BMD measurements, and summarize recent knowledge regarding the relationships between ‘low BMD’ and ‘fracture incidence, vascular calcification and increased mortality’ in ESRD patients, as well as potential ‘molecular mechanisms’ underlying these associations. Oxford University Press 2020-06-26 /pmc/articles/PMC7367137/ /pubmed/32699616 http://dx.doi.org/10.1093/ckj/sfaa089 Text en © The Author(s) 2020. Published by Oxford University Press on behalf of ERA-EDTA. http://creativecommons.org/licenses/by-nc/4.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com |
spellingShingle | CKJ Reviews Iseri, Ken Dai, Lu Chen, Zhimin Qureshi, Abdul Rashid Brismar, Torkel B Stenvinkel, Peter Lindholm, Bengt Bone mineral density and mortality in end-stage renal disease patients |
title | Bone mineral density and mortality in end-stage renal disease patients |
title_full | Bone mineral density and mortality in end-stage renal disease patients |
title_fullStr | Bone mineral density and mortality in end-stage renal disease patients |
title_full_unstemmed | Bone mineral density and mortality in end-stage renal disease patients |
title_short | Bone mineral density and mortality in end-stage renal disease patients |
title_sort | bone mineral density and mortality in end-stage renal disease patients |
topic | CKJ Reviews |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7367137/ https://www.ncbi.nlm.nih.gov/pubmed/32699616 http://dx.doi.org/10.1093/ckj/sfaa089 |
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