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
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

305-343

Informations de copyright

Copyright © 2022 Elsevier Inc. All rights reserved.

Auteurs

Aiji Yajima (A)

Department of Anatomy, Cell Biology and Physiology, Indiana University, School of Medicine, Indianapolis, IN, United States; Department of Urology, Tokyo, Teishin Hospital, Tokyo, Japan; Department Blood Purification, Kidney Center, Tokyo Women's Medical University, Tokyo, Japan. Electronic address: a-and-y@rj8.so-net.ne.jp.

Ken Tsuchiya (K)

Department Blood Purification, Kidney Center, Tokyo Women's Medical University, Tokyo, Japan.

Makoto Kuro-O (M)

Division of Anti-aging Medicine, Center for Molecular Medicine, Jichi Medical University, Shimotsuke, Japan.

Pablo Urena (P)

Division of Nephrology, Clinique du Landy, Saint Ouen, France.

Yoshihiro Tominaga (Y)

Department of Endocrine Surgery, Nagoya Daini Red Cross Hospital, Nagoya, Japan.

Manabu Okada (M)

Department of Endocrine Surgery, Nagoya Daini Red Cross Hospital, Nagoya, Japan.

Toshihiro Ichimori (T)

Department of Endocrine Surgery, Nagoya Daini Red Cross Hospital, Nagoya, Japan.

Toshihide Tomosugi (T)

Department of Endocrine Surgery, Nagoya Daini Red Cross Hospital, Nagoya, Japan.

Takahisa Hiramitsu (T)

Department of Endocrine Surgery, Nagoya Daini Red Cross Hospital, Nagoya, Japan.

Taro Murata (T)

Department of Urology, Tokyo, Teishin Hospital, Tokyo, Japan.

Masaki Nakamura (M)

Department of Nephrology and Urology, NTT East Kanto Hospital, Tokyo, Japan.

Masahiko Sasaki (M)

Department of Urology, Tokyo, Teishin Hospital, Tokyo, Japan.

Akemi Ito (A)

Ito Bone Histomorphometry Institute, Niigata, Japan.

Kosaku Nitta (K)

Department of Medicine, Kidney Center, Tokyo Women's Medical University, Tokyo, Japan.

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Classifications MeSH