Available online 22 July 2022
AbstractThe 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.
KeywordsRenal hyperparathyroidism
FGF-23
Parathyroid hormone
Calcium
Phosphorus
Vitamin D
Renal bone disease
Calcimimetic agents
Parathyroidectomy
View full textCopyright © 2022 Elsevier Inc. All rights reserved.
留言 (0)