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Background. Secondary hyperparathyroidism (SHPT) is universal complication of chronic kidney disease (CKD), the likelihood of which increases as renal function decreases. Currently, SHPT is considered in the context of mineral and bone disorders associated with CKD. Mineral and bone disorders associated with CKD include, in addition to SHPT, disorders of calcium-phosphorus metabolism, bone pathology and metastatic calcification, which determine poor outcomes of the disease. The purpose of the study was to evaluate the serum concentrations of fibroblast growth factor (FGF) 23 and Klotho protein in patients with various stages of CKD and their relationship with SHPT, vitamin D levels, and calcium-phosphorus metabolism in patients with varying degrees of decreased renal function. Materials and methods. Serum concentrations of FGF 23, Klotho protein, parathyroid hormone (PTH), 25(OH)D, calcium and phosphorus were evaluated in 229 patients with various stages of chronic kidney disease and in 40 people without signs of CKD. Results. It has been shown that individuals with CKD are characterized by overproduction of humoral phosphatonin FGF 23 and Klotho deficiency, which increase as renal failure worsens. A significant relationship was established between FGF 23 and the levels of PTH and blood phosphorus; Klotho protein — with the patient’s age and serum vitamin D. An early marker of disorders in the FGF 23-Klotho system is a decrease in the Klotho protein concentration, which occurs in the early stages of CKD and is aggravated with the progression of renal failure. A statistically significant overproduction of FGF 23 associated with secondary hyperparathyroidism was registered in patients with glomerular filtration rate less than 35 ml/min/1.73 m2. Conclusions. An early marker of disorders in the FGF 23-Klotho system is a decrease in the concentration of the Klotho protein, which occurs in the early stages of CKD and is aggravated with the progression of renal fai-
lure. The relationship between Klotho deficiency and the formation of SHPT has not been found. As kidney function decreases, excess production of PTH and FGF 23 appears and increases, hyperphosphatemia progresses. This proves the pathogenetic relationship between the formation of SHPT and the overproduction of humoral phosphatonin FGF 23, since it is this glomerular filtration rate that determines the growth of PTH above the upper limit of the general population reference interval.
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