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Citation
Tags
HERO ID
7287391
Reference Type
Journal Article
Subtype
Review
Title
Bone mineral density and mortality in end-stage renal disease patients
Author(s)
Iseri, K; Dai, L; Chen, Z; Qureshi, AR; Brismar, TB; Stenvinkel, P; Lindholm, B
Year
2020
Is Peer Reviewed?
Yes
Journal
Clinical Kidney Journal
ISSN:
2048-8505
EISSN:
2048-8513
Volume
13
Issue
3
Page Numbers
307-321
Language
English
PMID
32699616
DOI
10.1093/ckj/sfaa089
Web of Science Id
WOS:000577240400008
Abstract
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.
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