Chronic kidney disease (CKD) has been shown to impair the metabolism of a number of minerals, resulting in bone damage, vascular wall calcifications, functional disorders, and significant mortality. Renal osteodystrophy in this disease is characterized by histological bone abnormalities and altered rate of bone transformation (increased in fibrous osteitis or decreased in adynamic bone disease), pathological mineralization (osteomalacia), and bone loss. Secondary hyperparathyroidism (SHPT) is

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... sociated with fibrosis osteitis, early build-up of phosphorus (responsible for excess production of fibroblast growth factor-23 (FGF-23) by the bone tissue), decreased production of calcitriol by the kidneys and hypocalcemia. Other bone debilitating factors include acidosis, chronic inflammation, food deficiency, and iatrogenic complications. It has been proven that with the progression of CKD and the reduction of glomerular filtration, the activity of FGF-23 is increased, which leads to inhibition of alpha-1 hydroxylase and to decreased levels of 1,25 dihydroxyvitamin D. FGF-23 comes predominantly from the bones, while α-Klotho -from the kidneys, and together they play different important roles to maintain mineral metabolism. CKD is associated with significant increases in FGF-23 concentrations and inhibition of α-Klotho. Hyperphosphatemia, which correlates with endothelial dysfunction and elevated FGF-23, with an untimely treatment, results in pruritus, bone pain, anemia, cardiovascular complications, disability, and reduced survival rate. The association between protein-related uremic toxins and FGF-23 is a challenge motivating the study of bone biomarkers. Scr Sci Med. 2018;50(1):36-40