Phosphate and bone fracture risk in chronic kidney disease patients.
CKD
MBD
bone fractures
phosphate levels
Journal
Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association
ISSN: 1460-2385
Titre abrégé: Nephrol Dial Transplant
Pays: England
ID NLM: 8706402
Informations de publication
Date de publication:
20 02 2021
20 02 2021
Historique:
received:
07
05
2019
accepted:
29
08
2019
pubmed:
18
10
2019
medline:
18
5
2021
entrez:
18
10
2019
Statut:
ppublish
Résumé
In chronic kidney disease (CKD), phosphate homoeostasis plays a central role in the development of mineral and bone disorder (MBD) together with decreased serum calcium and elevated serum parathyroid hormone, fibroblast growth factor 23 and sclerostin levels. Today there are only a few data exploring the direct role of abnormal phosphate homoeostasis and hyperphosphataemia in the development of CKD-MBD. On the other hand, several studies have looked at the link between hyperphosphataemia and cardiovascular morbidity and mortality in CKD, but there is a lack of evidence to indicate that lowering phosphate levels improves cardiovascular outcomes in this population. Furthermore, the impact of liberalizing phosphate targets on CKD-MBD progression and bone fracture is currently not known. In this review we discuss the central role of phosphate in the pathogenesis of CKD-MBD and how it may be associated with fracture risk, both in hyper- and hypophosphataemia.
Identifiants
pubmed: 31620773
pii: 5588742
doi: 10.1093/ndt/gfz196
doi:
Substances chimiques
Phosphates
0
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
405-412Informations de copyright
© The Author(s) 2019. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved.