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[The pathophysiology of adynamic bone disease]
K Yokoyama1, T Shigematsu, Y Ogura
1Division of Nephrology and Hypertension, Tokyo Jikei University School of Medicine.
Insights
Adynamic bone disease, common in dialysis patients, shows reduced bone turnover. Skeletal resistance to parathyroid hormone (PTH) is a key factor, potentially involving PTH receptor downregulation.
Area of Science:
- Nephrology
- Endocrinology
- Bone Metabolism
Context:
- Adynamic bone disease is a prevalent skeletal complication in patients undergoing dialysis.
- It is characterized by markedly reduced bone turnover.
- It is nearly as prevalent as osteitis fibrosis in hemodialysis patients.
Purpose:
- To summarize the current understanding of adynamic bone disease pathophysiology in dialysis patients.
- To highlight the role of skeletal resistance to parathyroid hormone (PTH).
Summary:
- Adynamic bone disease, noted since the 1980s, is the predominant bone lesion in peritoneal dialysis patients.
- Unlike osteomalacia, it features reduced bone turnover without increased osteoid formation.
- Skeletal resistance to PTH's calcemic action is a crucial factor, with recent studies suggesting PTH receptor downregulation and osteoclast inhibitory factor involvement.
Impact:
- Provides insight into the pathophysiology of a common complication in dialysis patients.
- Highlights potential therapeutic targets related to PTH signaling and bone metabolism.
- Contributes to understanding bone disease management in chronic kidney disease.
Abstract:
Adynamic bone disease was first noted in the early 1980s. It now represents the predominant bone lesion in peritoneal dialysis patients and is nearly as prevalent as osteitis fibrosis in hemodialysis patients. Bone turnover is markedly reduced in this disorder but, A in contrast to osteomalacia, there is no increase in osteoid formation. Although the pathophysiology of adynamic bone disease is still obscure, skeletal resistance to the calcemic action of PTH is important factor. Recently several study, whose reveal the down regulation of PTH receptor, osteoclast inhibitory factor and a assay of PTH, whole PTH play a role on the pathophysiology of skeletal resistance, were reported.
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