ArticleClinical kidney journal2025
Pathophysiology and therapies of CKD-associated secondary hyperparathyroidism.
Article in Clinical kidney journal, 2025. 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.
- Serum calcium dynamics and risk of all-cause hospitalization and mortality in hemodialysis patients: a landmark analysis from the international DOPPS.Clinical kidney journal · 2026Article
- Article
- Low Time-Weighted Parathyroid Hormone Is Associated with Malnutrition-Inflammation and Functional Dependence in Maintenance Hemodialysis.Nutrients · 2026Article
- Unraveling the mystery of parathyroid oxyphil cells in uremic SHPT: ongoing challenges and multi-omics advances.Journal of molecular cell biology · 2026Review
- Calcimimetic and vitamin D receptor agonist therapy associates with lower mortality and fractures in hemodialysis patients: an international DOPPS analysis.Clinical kidney journal · 2026Article
- Extended-release calcifediol identifies a therapeutic vitamin D range in chronic kidney disease stages 3 and 4.Clinical kidney journal · 2026Article
- Pre-Parathyroidectomy PTH as an Integrated Biomarker of Glandular Remodeling and Skeletal Turnover in Secondary Hyperparathyroidism.International journal of molecular sciences · 2026Review
- Modeling Longitudinal Relationships Between CKD-MBD Biomarker Trajectories with Interpretable Machine Learning in a Large Prospective CKD Cohort.Journal of clinical medicine · 2026Article
- Endocrine disorders linked to chronic kidney disease: Mechanisms and clinical implications.World journal of nephrology · 2026Review
- Band keratopathy and conjunctival calcification in end-stage kidney disease: epidemiology, pathophysiology and clinical management.Clinical kidney journal · 2026Review
- Combination therapy with nutritional vitamin D and calcimimetics in secondary hyperparathyroidism: a mechanism-based approach to restoring PTH regulation.Frontiers in nutrition · 2026Review
- From deep learning discovery to clinical validation: a new composite marker predicts mortality in type 2 diabetes.Cardiovascular diabetology. Endocrinology reports · 2025Article
- Predictors of Hungry Bone Syndrome and Reintervention After Subtotal Versus Total Parathyroidectomy for Secondary Hyperparathyroidism in Dialysis Patients: A Single-Center Cohort.Journal of clinical medicine · 2025Article
- New perspectives on chronic kidney disease-mineral bone disorder.Clinical kidney journal · 2025Article
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Authors and funding
7 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Uremic secondary hyperparathyroidism (SHP) refers to the biochemical abnormalities that characterize CKD-MBD. However, historically parathyroid hormone (PTH) is identified as the key culprit hormone and the essential biomarker of secondary hyperparathyroidism. SHP represents the adaptive response to several mineral abnormalities that initiate and maintain increased PTH secretion through classical mineral derangements and more recently elucidated hormonal dysregulations. Among classic factors involved in the pathogenesis of SHP, phosphate, calcium, and calcitriol have a prominent role. The discovery of new pathogenetic factors involved in the development of SHP (and the eventual CKD-MBD) including fibroblast growth factor-23 (FGF23) and klotho provides new hypothesis and perspectives to our understanding of this complex metabolic disturbance. Recently more than serum phosphate a critical role in regulating FGF23 synthesis and the progression of CKD is ascribed to phosphate pool, reflected by production of glycerol-3-phosphate and the formation of excessive CPP-2. Finally, also skeletal resistance to PTH action, due to dysregulation of the Wnt-β-catenin system and intestinal dysbiosis, affecting the PTH actions on bone are causal factor of SHP. Identifying all the actors at play is mandatory to allow the most precise therapeutic prescription in the individual patient. This paper aims to review, in particular, the pathophysiology of SHP, which is essential to envisage the eventual therapeutic options for the associated MBD.
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