Author/Editor		Pečovnik-Balon, Breda; Ekart, Robert; Gorenjak, Maksimiljan
Title		Fibroblastni rastni faktor 23 in kronična ledvična bolezen
Translated title		Fibroblast growth factor 23 in chronic kidney disease
Type		članek
Source		In: Monografija IV. osteoloških dnevov z mednarodno udeležbo Maribor : Univerzitetni klinični center
Publication year		2013
Volume		str. 123-127
Language		slv
Abstract		Fibroblastni rastni factor 23 (FGF 23) je najpomembnejši uravnalec ravnovesja fosfatov (P). Deluje preko FGF receptorjev in koreceptorja Klotho. FGF 23 zavira ledvično 1 alfa hidroksilazo in pospešuje delovanje 24-hidroksilaze. Zmanjšuje izločanje parathormona (PTH). FGF 23 nastaja in se izloča iz osteocitov in osteoblastov pod vplivom aktivne oblike vitamina D in povečanega vnosa fosfatov s hrano. Najbolj značilno je povečano izločanje FGF 23 pri bolnikih s kronično ledvično boleznijo (KLB). V zgodnjih stopnjah KLB povišan FGF 23 pospešuje izločanje P in preprečuje nastanek hiperfosfatemije. Znižuje nivo aktivne oblike vitamina D in sodeluje pri nastanku sekundarnega hiperparatiroidizma. Pri bolnikih s končno obliko ledvične odpovedi (ESRD) je FGF 23 lahko zelo visok in je napovednik kostne mineralizacije, hipertrofije levega prekata, žilnih kalcifikacij in umrljivosti. Ugotoviti je treba ali je FGF 23 občutljiv biomarker fosfatnega ravnovesja ali ima učinek neodvisno od serumskega fosforja. Zmanjšanje biološke aktivnosti FGF 23 je lahko pomemben terapevtski ukrep.Fibroblast growth factor 23 (FGF-23) is likely to be the most important regulator of phosphate homeostasis, which mediates its functions through FGF receptors and the coreceptor Klotho. FGF 23 inhibits the renal 1-hydroxylase and stimulates the 24-hydroxylase, and it appears to reduce parathyroid hormone (PTH) secretion in short-term studies. FGF 23 synthesis and secretion by osteocytes and osteoblasts is upregulated through 1,25-dihydroxyvitamin D(3) [1,25(OH)(2)D(3)] and through an increased dietary phosphate intake. The most significant increases of FGF 23 are found in patients with chronic kidney disease (CKD). During the early stages of CKD, increased FGF 23 production enhances urinary phosphate excretion and thus prevents the development of hyperphosphatemia, reduces the circulating levels of 1,25(OH)(2)D(3), and therefore contributes to the development of secondary hyperparathyroidism. In patients with end-stager enal disease (ESRD), FGF 23 levels can be extremely high and were shown to be predictors of bone mineralization, left ventricular hypertrophy, vascular calcification, and mortality. It remains to be determined, however, whether FGF 23 represents simply a sensitive biomarker of an abnormal phosphate homeostasis or has, independent of serum phosphate levels, potentially negative off-target effects. Nonetheless, reducing the production and/or the biologic activity of FGF 23 may be an important therapeutic goal for this patient population.
Keywords		fibroblastni rastni faktor 23 fosfat fosfatni vezalci protitelesa fibroblast growth factor 23 phosphat phosphat binfers antibodies