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[Bone disease in chronic renal failure and its modern therapy]
1Klinika nefrologie, Transplantacní centrum IKEM Praha. sulkovas@volny.cz
Insights
Secondary hyperparathyroidism, a complication of chronic renal failure, impacts bone and cardiovascular health. Treatment focuses on correcting hyperphosphatemia and parathyroid gland activity using phosphate binders, calcimimetics, and vitamin D receptor activators.
Area of Science:
- Nephrology
- Endocrinology
- Bone Metabolism
Background:
- Renal bone disease is a severe complication of chronic kidney disease (CKD).
- Secondary hyperparathyroidism is a key factor in its development.
- CKD-MBD links bone disease and cardiovascular issues in renal patients.
Purpose of the Study:
- To outline current prevention and treatment strategies for renal bone disease.
- To highlight the interplay between bone and cardiovascular complications in CKD.
- To discuss the role of specific drug classes in managing CKD-MBD.
Main Methods:
- Review of pathogenetic and clinical interrelationships in CKD-MBD.
- Focus on correcting hyperphosphatemia and parathyroid gland overactivity.
- Utilizing vitamin D receptor (VDR) and calcium receptor (CaR) modulation.
Main Results:
- Treatment prioritizes correcting hyperphosphatemia.
- Subsequent management targets parathyroid gland reactivity.
- Key drug classes include GIT phosphate binders, calcimimetics, and VDR activators.
Conclusions:
- Effective management of CKD-MBD requires addressing both bone and cardiovascular aspects.
- Pharmacological interventions targeting VDR and CaR are crucial.
- Specific therapies exist for refractory cases and calciphylaxis.
Abstract:
Renal bone disease is one of the most serious complications of chronic renal failure. Secondary hyperparathyreosis is decisive for its pathogenesis. Current prevention and treatment emphasises pathogenetic and clinical interrelationships between bone tissue involvement and cardiovascular complications (CKD-MBD, bone and venous involvement associated with chronic renal disease). The treatment should first correct hyperphosphatemia and, subsequently, hyperreactivity of parathyroid glands through vitamin D receptor (VDR) and calcium receptor (CaR) modulation. Three groups of drugs play a fundamental role here (GIT phosphate binders, calcimimetics and vitamin D receptor activators). Certain other therapeutic approaches are used in some specific situations such as, among others, refractory hyperparathyreosis or calciphylaxis.
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