Cargando…

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...

Descripción completa

Detalles Bibliográficos
Autores principales: Iseri, Ken, Dai, Lu, Chen, Zhimin, Qureshi, Abdul Rashid, Brismar, Torkel B, Stenvinkel, Peter, Lindholm, Bengt
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Oxford University Press 2020
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
_version_ 1783560361110142976
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
work_keys_str_mv AT iseriken bonemineraldensityandmortalityinendstagerenaldiseasepatients
AT dailu bonemineraldensityandmortalityinendstagerenaldiseasepatients
AT chenzhimin bonemineraldensityandmortalityinendstagerenaldiseasepatients
AT qureshiabdulrashid bonemineraldensityandmortalityinendstagerenaldiseasepatients
AT brismartorkelb bonemineraldensityandmortalityinendstagerenaldiseasepatients
AT stenvinkelpeter bonemineraldensityandmortalityinendstagerenaldiseasepatients
AT lindholmbengt bonemineraldensityandmortalityinendstagerenaldiseasepatients