[Serum troponin-I as a marker of fibroblast growth factor-23 (FGF-23) cardiotoxic effect, in patients with chronic kidney disease].

Autor:	Taranova MV; Sechenov First Moscow State Medical University of the Ministry (Sechenov University)., Milovanova LY; Sechenov First Moscow State Medical University of the Ministry (Sechenov University)., Kozlovskaya Lysenko LV; Sechenov First Moscow State Medical University of the Ministry (Sechenov University)., Milovanova SY; Sechenov First Moscow State Medical University of the Ministry (Sechenov University)., Androsova TV; Sechenov First Moscow State Medical University of the Ministry (Sechenov University)., Zubacheva DO; Sechenov First Moscow State Medical University of the Ministry (Sechenov University)., Lebedeva MV; Sechenov First Moscow State Medical University of the Ministry (Sechenov University)., Dobrosmyslov IA; Sechenov First Moscow State Medical University of the Ministry (Sechenov University)., Kozlov VV; Sechenov First Moscow State Medical University of the Ministry (Sechenov University)., Kuchieva AM; Sechenov First Moscow State Medical University of the Ministry (Sechenov University)., Li OA; Sechenov First Moscow State Medical University of the Ministry (Sechenov University)., Reshetnikov VA; Sechenov First Moscow State Medical University of the Ministry (Sechenov University).
Jazyk:	ruština
Zdroj:	Terapevticheskii arkhiv [Ter Arkh] 2019 Jun 15; Vol. 91 (6), pp. 85-92. Date of Electronic Publication: 2019 Jun 15.
DOI:	10.26442/00403660.2019.06.000253
Abstrakt:	Aim: It has been established that an increased fibroblast growth factor (FGF-23) serum levels significantly contribute to the heart and blood vessels remodeling in patients with chronic kidney disease (CKD). But the precise mechanisms of the FGF-23 cardiac effect are currently being actively studied. At the same time, it is believed that the cardiac effects of FGF-23 may be due to the increasing deficit of Klotho protein as CKD progresses. In parallel with these changes, a number of studies indicate the persistence of the detectable troponins serum levels in CKD patients, even in the absence of clear clinical manifestations of cardiovascular diseases (CVD). The aim of the study was to confirm / exclude the existence of a causal relationship between elevated FGF-23, reduced Klotho and elevated troponin-I (as the most specific troponin in CKD). Materials and Methods: The study included 130 CKD stages 1-5D patients without clinically pronounced symptoms of СVD (Coronary artery disease, CCS class 2-4, Chronic heart failure, NYHA 24, myocarditis, pericarditis, arrhythmias), as well as the severe arterial hypertension (BP >160/90 mm Hg), according to the laboratory and instrumental methods of examination. The selected group of patients was studied: serum levels of FGF-23 (Human FGF-23 ELISA kit), Klotho (Human soluble Klotho with antiklotho monoclonal antibodies), troponin-I (high - sensitive assay), and also data from instrumental examination methods: electrocardiography (ECG), echocardiography (left ventricular myocardial mass index (LVMI), cardiac (valvular) calcification score (CCS) using a semi - quantitative point scale), sphygmagraphy (augmentation (stiffness) indices of vessels (AI), pulse wave velocity (PWV), central (aortic) blood pressure (CBP), blood supply of subendocardium (BSE) - using "Shygmacor" device (Australia)). Results and Discussion: The changes in serum levels of FGF-23, Klotho and troponin-I (Tr-I) depended on the stage of CKD. The following correlations were identified: FGF-23 and: Tr-I (r=0.601; p.
Databáze:	MEDLINE
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