TSUCHIYA Ken    Department   School of Medicine(Tokyo Women's Medical University Hospital), School of Medicine    Position   Professor (Fixed Term)
Article types	Original article
Language	English
Peer review	Non peer reviewed
Title	Renal hyperparathyroidism.
Journal	Formal name：Vitamins and hormones Abbreviation：Vitam Horm ISSN code：00836729/00836729
Volume, Issue, Page	120,pp.305-343
Author and coauthor	Yajima Aiji, Tsuchiya Ken, Kuro-O Makoto, Urena Pablo, Tominaga Yoshihiro, Okada Manabu, Ichimori Toshihiro, Tomosugi Toshihide, Hiramitsu Takahisa, Murata Taro, Nakamura Masaki, Sasaki Masahiko, Ito Akemi, Nitta Kosaku
Authorship	2nd author
Publication date	2022/07/22
Summary	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.
DOI	10.1016/bs.vh.2022.04.010
PMID	35953115