The study aimed to assess serum Klotho protein level in type 2 diabetic patients depending on kidney function. Methods. This observational study included 72 patients with diabetes mellitus (DM) and 26 patients with acute coronary syndrome. The control group consisted of 20 healthy subjects. Depending on the presence of albuminuria and glomerular filtration rate (GFR), the diabetics were divided into the following groups: group I included the patients with normal GFR and without albuminuria (n = 25); group ІІ consisted the patients with normal GFR and albuminuria (n = 23); group III – the patients with reduced GFR and albuminuria (n = 24) and group ІV included the patients with acute coronary syndrome (n = 26). The GFR was calculated using the CKD EPI formula (KDIGO 2012). The concentration of Klotho protein was determined by enzyme-linked immunosorbent assay. Results. The development of diabetic nephropathy in type 2 diabetic patients accompanied by a significant decrease of soluble Klotho compared with the controls and the patients of the1-st group. The level of Klotho protein in the group of patients with albuminuria decreased to (490.66 ± 58.76) pg/ml (p <0.05). The lowest concentration of Klotho (443.58 ± 46.92) pg/ml was found in the advanced stages of diabetic nephropathy, namely in patients with albuminuria and impaired renal function. Moreover, a significantly decreased serum Klotho was observed in acute coronary syndrome group in comparison with the control group (p <0.05). There were inverse correlations of Klotho concentration with urinary albumin and blood creatinine levels and a direct correlation between Klotho and GFR. Conclusions. The obtained data indicated the key role of Klotho protein in the formation of renal pathology in type 2 diabetes and the feasibility of practical use of Klotho determination as an early diagnostic marker of renal disorders and cardiovascular risk assessment. The strategies improving Klotho production may be useful in the reduction of both renal and vascular lesions progression in type 2 diabetic patients.

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Predicting the course of heart failure (HF) is an urgent task of modern medical science. Given the increasing prevalence of the disease with age, it is necessary to take into account the presence of comorbid pathology. The aim of the research was to study the relationship between gene polymorphisms of the β-adrenoceptor system with non-toxic goiter (NTG) and the HF course. Materials and methods. The total of 285 patients with HF against the background of post-infarction cardiosclerosis were included into the study. Of these, 158 (55.42%) patients had a comorbidly unfavorable pathology - NTG. Genotyping of 4 polymorphisms (Gly389Arg of the β1-adrenoreceptor gene, Ser49Gly gene of the β1-adrenoceptor (β1-AP) gene, Gln27Glu of the β2-AP gene and Ser275 of the β3- G-protein subunit gene was performed usingpolymerase chain reaction (PCR). Genetic and epidemiological analysis was performed using the SNPStats software. The obtained results. The presence of the G-allele of the Ser49Gly polymorphism of the β1-AP gene is associated with an increase in the rate of NTG development (recessive heredity model, x2 = 3.719, p = 0.039). We found a tendency to the increase of NTG development rate (by 5.9%) in the presence of the allele C polymorphism of Ser275 gene GNβ3 (recessive model of heredity, x2 = 3,452, p = 0,068). The risk of "low triiodothyronine" syndrome development in patients with HF, running against the background of NTG increases in homozygotes (G / G) according to the polymorphism Ser49Gly (c, 145A> G) of the β1-AR gene (odds ratio (OR) = 9.19 (3.69-22.90), g = 0.044). In patients with HF, which runs against the background of NTG, with the presence of the G allele polymorphism Gln27Glu (c, 79C> G) of the β2-AP gene, the risk of reaching a combined endpoint within two years (OR = 3.05 (1.10-8.43) increases in a homozygous state and OR= 3.38 (1.47-7.82) in heterozygotes, at p = 0.008), the risk also increases with heterozygous (G / C) patients with the Gly389Arg (c, 1165G> C) polymorphism of the β1-AR gene in the presence of NTG (OR = 2.09 (1.00-4.37), p = 0.046). Conclusion. Congenital genetic differences in -adrenoceptor pathways may be associated with the development of non-toxic goiter and the long-term course of heart failure.

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