Renal hyperparathyroidism.
Calcimimetic agents
Calcium
FGF-23
Parathyroid hormone
Parathyroidectomy
Phosphorus
Renal bone disease
Renal hyperparathyroidism
Vitamin D
Journal
Vitamins and hormones
ISSN: 0083-6729
Titre abrégé: Vitam Horm
Pays: United States
ID NLM: 0413601
Informations de publication
Date de publication:
2022
2022
Historique:
entrez:
11
8
2022
pubmed:
12
8
2022
medline:
16
8
2022
Statut:
ppublish
Résumé
The number of the patients with chronic kidney disease is now increasing in the world. The pathophysiology of renal hyperparathyroidism is closely associated with Klotho-FGF-endocrine axes, which must be solved definitively as early as possible. It was revealed that the expression of fgf23 is activated by calciprotein particles, which induces vascular ossification. And it is well known that phosphorus overload directly increases parathyroid hormone and hyperparathyroid bone disease develops in those subjects. On the other hand, low turnover bone disease is often recently. Both the patients with chronic kidney disease suffering from hyperparathyroid bone disease or low turnover bone disease are associated with increased fracture risk. Micropetrosis may be one of the causes of increased fracture risk in the subjects with low turnover bone disease. In this chapter, we now describe the diagnosis, pathophysiology and treatments of renal hyperparathyroidism.
Identifiants
pubmed: 35953115
pii: S0083-6729(22)00056-5
doi: 10.1016/bs.vh.2022.04.010
pii:
doi:
Substances chimiques
Parathyroid Hormone
0
Calcium
SY7Q814VUP
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
305-343Informations de copyright
Copyright © 2022 Elsevier Inc. All rights reserved.