Altynay Balmukhanova, Assiya Kanatbayeva, K. Kabulbayev, Maxsot Karasayev, D. Batyrbayeva
{"title":"The significance of Fibroblast growth factor 23 (FGF-23) in humans","authors":"Altynay Balmukhanova, Assiya Kanatbayeva, K. Kabulbayev, Maxsot Karasayev, D. Batyrbayeva","doi":"10.31082/1728-452x-2020-217-218-7-8-37-43","DOIUrl":null,"url":null,"abstract":"Nowadays chronic kidney disease (CKD) is one of the leading chronic non-communicable diseases in terms of morbidity and mortality. One of the most serious complications is mineral-bone disorder, which worsen the clinical course and prognosis of patients. Fibroblast growth factor 23 (FGF-23) is a new biomarker that regulates phosphate metabolism and plays an important role in the pathogenesis of many complications in CKD. Purpose. To study the physiological role of FGF-23, as well as its potential clinical significance in the progression of CKD and its complications. Material and methods. A 20-year-deep literature search was conducted in the international scientific databases PubMed / Medline, Web of Science and Google Scholar for the following keywords: \"Fibroblast growth factor 23\", \"FGF-23\", \"phosphate homeostasis\", \"chronic kidney disease\", \"Mineral and bone disorders\", \"left ventricular hypertrophy\". Results and discussion. FGF-23 is a protein secreted by bone cells and its primary physiological role is to regulate urinary excretion of phosphate to maintain a stable level in serum. Moreover, FGF-23 decreases calcitriol levels and inhibits parathyroid hormone secretion. In CKD, there is a gradual increase in FGF-23 levels as renal function declines, which can be regarded as physiological compensation to stabilize serum phosphate levels. According to the several studies, FGF-23 might be associated with cardiovascular complications, such as left ventricular hypertrophy and heart failure. Conclusion. Thus, FGF-23 is not only a marker of mineral-bone disorders in CKD, but also a key link in the pathogenesis of the development of secondary hyperparathyroidism and cardiovascular complications. With this in mind, FGF-23 may represent a multifunctional therapeutic target that may improve the prognosis of patients with CKD. Keywords: fibroblast growth factor-23, phosphate, parathyroid hormone, left ventricular hypertrophy, mineral-bone disorder.","PeriodicalId":14842,"journal":{"name":"Journal \"Medicine\"","volume":"7 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2021-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal \"Medicine\"","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.31082/1728-452x-2020-217-218-7-8-37-43","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Nowadays chronic kidney disease (CKD) is one of the leading chronic non-communicable diseases in terms of morbidity and mortality. One of the most serious complications is mineral-bone disorder, which worsen the clinical course and prognosis of patients. Fibroblast growth factor 23 (FGF-23) is a new biomarker that regulates phosphate metabolism and plays an important role in the pathogenesis of many complications in CKD. Purpose. To study the physiological role of FGF-23, as well as its potential clinical significance in the progression of CKD and its complications. Material and methods. A 20-year-deep literature search was conducted in the international scientific databases PubMed / Medline, Web of Science and Google Scholar for the following keywords: "Fibroblast growth factor 23", "FGF-23", "phosphate homeostasis", "chronic kidney disease", "Mineral and bone disorders", "left ventricular hypertrophy". Results and discussion. FGF-23 is a protein secreted by bone cells and its primary physiological role is to regulate urinary excretion of phosphate to maintain a stable level in serum. Moreover, FGF-23 decreases calcitriol levels and inhibits parathyroid hormone secretion. In CKD, there is a gradual increase in FGF-23 levels as renal function declines, which can be regarded as physiological compensation to stabilize serum phosphate levels. According to the several studies, FGF-23 might be associated with cardiovascular complications, such as left ventricular hypertrophy and heart failure. Conclusion. Thus, FGF-23 is not only a marker of mineral-bone disorders in CKD, but also a key link in the pathogenesis of the development of secondary hyperparathyroidism and cardiovascular complications. With this in mind, FGF-23 may represent a multifunctional therapeutic target that may improve the prognosis of patients with CKD. Keywords: fibroblast growth factor-23, phosphate, parathyroid hormone, left ventricular hypertrophy, mineral-bone disorder.