ReviewJournal of endocrinological investigation2026
Chronic kidney disease: from mineral dysregulation to bone and cardiovascular disease.
Review in Journal of endocrinological investigation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
6 authors.
Funding
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Abstract
backgroundChronic kidney disease-mineral bone disorder (CKD-MBD) concerns more than 50% of patients with moderate/severe CKD, increasing their risk for fractures and cardiovascular events. PURPOSE: To present its pathogenesis, clinical presentation and management.
methodsA Pubmed search for CKD-MBD until December 2025 was conducted using combinations of relevant terms.
resultsTotal-body positive phosphate balance, increased levels of fibroblast-growth factor 23 (FGF-23) and sclerostin, and bone resistance to parathyroid hormone (PTH) are the earliest detected abnormalities, followed by calcitriol deficiency, secondary hyperparathyroidism, and bone minerals derangement. High bone turnover and adynamic bone disease stem from PTH excess and deficiency/resistance respectively, with the latter being prevalent in early CKD, peritoneal dialysis and post-kidney transplantation. Osteomalacia is rare, while mixed uremic osteodystrophy is rather common. Fracture risk assessment is based on fracture risk assessment tool, bone mineral density testing and vertebral morphometry, while bone biopsy remains the gold standard for renal osteodystrophy evaluation. Cardiovascular manifestations include vascular calcifications and left ventricular hypertrophy induced by mineral stress in the setting of disrupted buffering system, osteoblastic differentiation of vascular smooth cells and direct FGF-23 effects in myocardium. In severe secondary hyperparathyroidism, active vitamin D and analogues, calcimimetics, and, in refractory cases, parathyroidectomy effectively lower PTH. In mild/moderate CKD, the efficacy of all anti-osteoporotic agents is mainly proven in post-menopausal women without biochemical evidence of CKD-MBD. In dialysis patients, denosumab is the best-studied agent, while recent data highlight pronounced therapeutic benefit of romosozumab. Finally, teriparatide has demonstrated utility in treating adynamic bone disease.
conclusionsFracture risk prevention in CKD-MBD should be prioritized. Dedicated research and validation of CKD-specific bone turnover markers may assist towards this direction.
Indexed as
Identifiers
42501286What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.