ReviewEndocrinology and metabolism (Seoul, Korea)2024
Roles of Parathyroid Hormone and Fibroblast Growth Factor 23 in Advanced Chronic Kidney Disease.
Review in Endocrinology and metabolism (Seoul, Korea), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
- Bone turnover markers associated with cognitive dysfunction in patients undergoing hemodialysis: a cross-sectional study.JBMR plus · 2026Article
- Role of fibroblast growth factor-23 in renal disease activity and bone density involvement in patients with lupus nephritis.World journal of nephrology · 2026Article
- Association Between Serum Parathyroid Hormone Levels and Femoral Bone Mineral Density in Patients with Chronic Kidney Disease Stage 3.Journal of clinical medicine · 2026Article
- Pre-Parathyroidectomy PTH as an Integrated Biomarker of Glandular Remodeling and Skeletal Turnover in Secondary Hyperparathyroidism.International journal of molecular sciences · 2026Review
- Allopurinol has no effect on calcitriol or other CKD-MBD biomarkers: a randomized double-blind study.Journal of the Endocrine Society · 2026Article
- Diabetes progression and its association with fracture risk in type 2 diabetes.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2026Article
- Endocrine disorders linked to chronic kidney disease: Mechanisms and clinical implications.World journal of nephrology · 2026Review
- Heterogeneous regulation of fibroblast growth factor 23 in acute kidney injury, chronic kidney disease, and polycystic kidney disease: mechanisms, diagnostic utility, and clinical implications.Frontiers in molecular biosciences · 2026Review
- Combination therapy with nutritional vitamin D and calcimimetics in secondary hyperparathyroidism: a mechanism-based approach to restoring PTH regulation.Frontiers in nutrition · 2026Review
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- Article
- Treatment outcomes and determinants of combined hemodialysis-hemoperfusion therapy in chronic glomerulonephritis.American journal of translational research · 2025Article
- Immune mechanisms in chronic kidney disease-mineral and bone disorder: current insights and therapeutic implications.Frontiers in medicine · 2025Review
- Association of RAGE gene polymorphisms (rs2070600 and rs2071288) with bone metabolism disturbances in patients with chronic kidney disease.International journal of molecular and cellular medicine · 2025Article
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Parathyroid hormone (PTH) and fibroblast growth factor 23 (FGF23) each play a central role in the pathogenesis of chronic kidney disease (CKD)-mineral and bone disorder. Levels of both hormones increase progressively in advanced CKD and can lead to damage in multiple organs. Secondary hyperparathyroidism (SHPT), characterized by parathyroid hyperplasia with increased PTH secretion, is associated with fractures and mortality. Emerging evidence suggests that these associations may be partially explained by PTH-induced browning of adipose tissue and increased energy expenditure. Observational studies suggest a survival benefit of PTHlowering therapy, and a recent study comparing parathyroidectomy and calcimimetics further suggests the importance of intensive PTH control. The mechanisms underlying the regulation of FGF23 secretion by osteocytes in response to phosphate load have been unclear, but recent experimental studies have identified glycerol-3-phosphate, a byproduct of glycolysis released by the kidney, as a key regulator of FGF23 production. Elevated FGF23 levels have been shown to be associated with mortality, and experimental data suggest off-target adverse effects of FGF23. However, the causal role of FGF23 in adverse outcomes in CKD patients remains to be established. Further studies are needed to determine whether intensive SHPT control improves clinical outcomes and whether treatment targeting FGF23 can improve patient outcomes.
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