Chronic kidney disease: from mineral dysregulation to bone and cardiovascular disease
Abstract
Background: Chronic 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.
Methods: A Pubmed search for CKD-MBD until December 2025 was conducted using combinations of relevant terms.
Results: Total-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…
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