HORMONAL REGULATION OF SA-P EXCHANGE IN PATIENTS WITH CHRONIC KIDNEY DISEASE AND THERAPEUTIC APPROACHES TO CORRECTION
Introduction. One of the most frequent and difficult problems arising in the treatment of dialysis patients is the correction of phosphorus-calcium metabolism. In chronic renal failure, all links of phosphorus-calcium metabolism are disrupted. With a decrease in the glomerular filtration rate (GFR) below 60 ml / min / 1.73 m2, the filtration of phosphorus decreases and its concentration in the blood serum increases, which causes an increase in the secretion of parathyroid hormone (PTH).
Goal. To summarize the information about the role of hormonal regulation of phosphorus-calcium metabolism in the pathogenesis of chronic kidney disease and cardiovascular diseases, it is accompanied, and to analyze the main therapeutic approaches for the correction of these disorders.
Materials and methods. Bibliographic - a theoretical analysis is carried out and a generalization of literature data is carried out, the actual content is analyzed. In the study, a questionnaire-survey method was used, as well as description, analysis, abstracting.
Results and discussion. PTH is produced by the main cells of the parathyroid glands (PTH). Serum Ca2+ concentration is the main modulator of PTH secretion . Stimulation of the calcium-sensitive receptors (CSR) of the thyroid gland through a cascade of reactions ultimately leads to the suppression of PTH secretion. An additional stimulus for an increase in PTH secretion is hyperphosphatemia. PTH has the following physiological effects: stimulates the resorption of calcium from bone tissue, reabsorption of calcium in the renal tubules. Vitamin D (D3 and D2), in association with vitamin D-binding protein, is transported to the liver, where it is hydroxylated to form 25 (OH) D or calcidiol (KD), which then undergoes 1α-hydroxylation in the renal tubules, turning into the active form of the vitamin D is calcitriol (KT) or D-hormone. Protein Klotho is a transmembrane protein that, among other effects, provides some degree of insulin sensitivity and slows down the aging process in animal experiments. FGF23 has a phosphaturic effect, stimulates the secretion of PTH and inhibits the 1α-hydroxylase activity of the kidneys, leading to a decrease in the synthesis of QD and its level in the blood serum.
Conclusions. Elevated FGF23 and PTH levels are responsible for the adverse effects of excess phosphate, but inhibition of these compensatory mechanisms is clinically impossible as it leads to dangerous changes in mineral metabolism. At the same time, the prevention of cardiovascular complications in persons with disorders in the FGF23/Klotho system should include correction of the phosphate content, since their atherogenic role has been demonstrated, and attempts to reduce the absorption of phosphates using only phosphate binders can lead to an increase in the absorption of phosphates at a time when phosphate binders are not present in the intestinal cavity. Possibly one therapeutic approach in these patients is dietary control of Ca, P and vitamin D levels with blockade of intestinal active phosphate transport to reduce dietary phosphate absorption.
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