The aim: to evaluate functional and structural changes in blood vessels and myocardium in Wistar rats at different stages of the formation of experimental kidney dysfunction.Materials and Methods. Four groups of animals were studied. The first two groups consisted of rats subjected to 5/6 nephrectomy (NE). The period after NE is 2 or 4 months. The third and fourth groups included sham-operated (SO) animals of a similar observation period. After the end of the experiment, blood pressure was measured in rats, the left ventricular mass index (LVMI) was calculated, a biochemical blood test, histological, immunohistochemical and electron microscopic examination of the myocardium were performed, and the contractile activity of the portal vein was recorded for a period of 2 months (in vitro).Results. 2 months after NE, an increase in blood pressure, LVMI, and a decrease in the autorhythmic contractile activity of the portal vein were detected in rats. At the histological level, thickening of cardiomyocytes and arterial vessel walls and the presence of perivascular fibrosis were noted. After 4 months, in rats with NE, the increase in blood pressure, cardiomyocyte hypertrophy and perivascular fibrosis progressed. The thickness of cardiomyocytes was 14.1±3.11 μm, which was significantly greater than in the group with NE for 2 months (12.5±1.5 μm; p=0.008). At this period of observation, electron microscopic examination revealed deintegration of myofibrils, disruption of myofibril stacking and z-disk structure, and changes in the shape of mitochondria. 2 months after NE, an increase in the area of open capillaries was detected in rats (1902.8±202.9 μm²) compared to the corresponding LO animals (730.4±58.2 μm²; p=0.000). As renal dysfunction develops, the capillary area tends to increase (2139.1±396.5 μm²; p =0.120).Conclusion. In Wistar rats with renal dysfunction, changes were detected not only in the level of blood pressure, but also in the functional activity of the intravenous fluid, as well as in the structural components of the myocardium – cardiomyocytes, stroma and blood vessels. The increase in myocardial mass at the histological level was manifested by a significant increase in the thickness of cardiomyocytes, the volume of connective tissue, and the thickness of the wall of arterial vessels, reaching a maximum value at a longer period after NE.

BACKGROUND. Dietary adjustment is an important point in the treatment of chronic kidney disease (CKD). However, at present, the effect of a diet with a high NaCl content on the state of the cardiovascular system in patients with early stages of CKD has not been sufficiently studied. The AIM: to evaluate blood pressure levels and changes in the myocardium of Wistar rats with early stage renal dysfunction fed a high-salt diet for a long time. MATERIALS AND METHODS: The study was performed on male Wistar rats. The control group consisted of sham-operated animals (LO-group), receiving a standard diet (0.34 % NaCl), the second – rats subjected to resection of ¾ of the kidney parenchyma, receiving a standard diet (NE-group), the third – rats, subjected to ¾ NE, receiving high sodium diet (4 % NaCl, NE+HSD). After 4 months, the rats were assessed for blood pressure (BP), levels of urea, creatinine, sodium in the blood serum, daily diuresis, albumin content in the urine, myocardial mass index (IMM) and left ventricular myocardial mass index (IMLV), and a histological examination of the myocardium was performed. RESULTS: In rats with kidney dysfunction, an increase in blood pressure was detected, most pronounced in the NE+HSD group. In rats of this group, albumin excretion, connective tissue volume, arterial diameter, thickness of the adventitia and media of myocardial vessels increased relative to the indicators of rats with NE receiving a standard diet. IMLV in NE+HSD rats was higher by 16.4 %, and IMM by 10.9 % than in animals with NE on a standard diet. The groups with NE did not differ from each other in the content of urea and creatinine in the blood serum, although these indicators were higher than in LO animals. There were no differences between groups in serum sodium levels. CONCLUSION: Prolonged consumption of a diet with a high content of table salt contributes to the development of the initial stages of CKD in Wistar rats, promotes blood pressure growth and myocardial remodeling, manifested primarily in the progression of cardiomyocyte hypertrophy and myocardial fibrosis.

Excessive salt intake is accompanied by the development of cardiovascular disorders, not always associated with an increase in blood pressure (BP). Given the cardioprotective effect of soy proteins in chronic kidney disease, the question arose of the possibility of leveling dietary interventions, in particular soy proteins, the damaging effect of a high-salt diet on the cardiovascular system. The aim of this work is to study the effect of long-term use of a diet high in NaCl and soy protein on myocardial remodeling and skin histomorphology in monkeys. The study was performed on male Javan macaques (Macaca fascicularis). The control group received a standard diet (2 g NaCl/kg feed). The second was a high-salt diet (8 g NaCl/kg feed), the third was a high-salt diet and SUPRO760 soy protein (200 g/kg feed). Echocardiography, registration of BP and heart rate were performed at baseline, after 4 and 12 months. After 12 months, a histological examination of the musculocutaneous flap was performed. In all animals, BP and heart rate did not change significantly during 12 months. In macaques on a high-salt diet, by the end of the study, deterioration in systolic and diastolic functions of the left ventricle (LV) was noted. In animals receiving additional soy protein, these changes leveled out. After 12 months, macaques fed soy protein had LV myocardial mass smaller and higher LV contractility than animals fed excess salt without soy protein. In monkeys on a high-salt diet, accumulation of collagen fibers in the hypodermis, hyalinization of the cytoplasm of capillary smooth muscle cells, perivascular and perineural edema of the reticular dermis were revealed. In animals treated with soy protein, skin capillary remodeling was less pronounced. Thus, high salt intake leads to adverse structural and functional disorders of the heart and blood vessels in cynomolgus monkeys, not associated with an increase in blood pressure. The inclusion of soy isolate in the diet reduces the negative effects of a high-salt diet on the cardiovascular system.

The relationship between dietary sodium, hypertension, and cardiovascular injury is far from clear. One of the important links in this process can be microRNAs that have the ability to modulate gene expression at the post-transcriptional level. However, their role in this process has not been fully studied. In addition, further studies require the identification of structural changes in the myocardium in conditions of long-term consumption of a high-salt diet. The aim of the study was to evaluate the expression levels of nuclear transcription factor κB (NFκB), microRNA (miRNA)-21 and structural changes in the myocardium during long-term consumption of a diet containing 8% (high) sodium chloride in Wistar rats. Material and methods. 20 Wistar rats with initial body weight 280.5±42.7 g were divided into two equal groups. The high salt (HS) group received 8% NaCl in the diet, the control (NS) group received the standard diet (0.34% NaCl). After 4 months, systolic blood pressure was measured in rats using the cuff method on the tail; the myocardial mass index was assessed after dissection; histological and electron microscopic examination of the myocardium was performed, and the expression levels of miRNA-21 and NFκB in the myocardium were determined. Results and discussion. Consumption of a diet high in sodium chloride for 4 months did not significantly affect the level of systolic blood pressure in normotensive Wistar rats, but led to an increase in myocardial mass index by 25.0% (p<0.05). In the HS group, hypertrophy of cardiomyocytes and an increase in the wall thickness of arterial vessels were revealed. The area of perivascular fibrosis in rats of the HS-group was almost 1.8 fold higher than in the NS-group. In animals of HS-group, the relative levels of expression of NFκB (more than 2 times) and miRNA-21 (almost 6 times) increased compared with the control. It can be assumed that the negative impact on the cardiovascular system of high-salt diets is partially realized through NFκB-associated signaling pathways and miRNA-21 activation. Conclusion. In Wistar rats, long-term use of a high-salt diet results in myocardial remodeling that is not associated with changes in blood pressure. At the same time, the adverse effects of high salt intake on the myocardium are mediated, in particular, by postgenomic mechanisms, namely an increase in the expression levels of NFκB and microRNA-21.

THE AIM: to evaluate the effect of a high-salt diet on the level of miRNA expression in urine and the mechanisms of endothelium-dependent vascular dilatation in rats. MATERIALS AND METHODS: 20 Wistar rats were divided into two equal groups. The high salt (HS) group received 8 % NaCl in the diet, the control (NS) received the standard diet (0.34 % NaCl). After 4 months, blood pressure (BP), left ventricular mass index (IMLV) were assessed in rats, and relative expression levels of miRNA-21, miRNA-133, and miRNA-203 were determined in urine. The reactivity of the rings of the aorta and the superior mesenteric artery (SMA) to acetylcholine (ACh) was assessed in vitro in isometric mode. RESULTS: there was no significant difference between the groups in terms of mean blood pressure (p> 0.05). However, in HS-rats an increase in IMLV was noted. The relative levels of expression of miRNA-21, miRNA-133, and miRNA-203 in the urine of rats fed a high-salt diet increased significantly as compared to the values of control animals. A high-salt diet resulted in a decrease in the reactivity of vascular segments precontracted with phenylephrine to ACh. A high-salt diet resulted in a decrease in the reactivity of vascular segments precontracted with phenylephrine to ACh. In the HS-group, the decrease in the amplitude of vasodilation under the action of ACh under conditions of blockade of NO-synthase (with the use of L-NIO) was less compared to the reaction in the absence of the blocker, than the NS-group: in the SMA of the HS group – by 45 %, NS group – by 69.4 %, in the aorta HS-group – by 49.4 %, NS-group – by 80.7 %. In contrast to the aorta, blockade of Ca2+-sensitive K+-channels in SMA (under the conditions of administration of tetraethylammonium, TRAM-34, or apamin) weakened ACh-induced relaxation, and in HS-rats, the decrease in vasodilation was more pronounced. CONCLUSION: consumption of a high-salt diet, without changing blood pressure, increases IMLV and the level of miRNA expression in the urine, and also reduces endothelium-dependent vascular relaxation, mediated, in particular, by impaired endothelial NO production, which is more pronounced in the aorta than in the SMA.

THE AIM: to evaluate the effect of low protein diet supplemented with ketosteril on morphological and epigenomic changes in the myocardium of Wistar rats with simulated kidney dysfunction . MATERIALS AND METHODS. The work was performed on male Wistar rats subjected to 5/6 nephrectomy (NE). The first group after NE received a standard diet (20.16% animal protein ), the second – low protein diet (LPD), including 10% ketosteril . Control rats received a standard diet . After 4 months , blood pressure (BP) and left ventricular mass index (LVMI) were assessed in rats , and a histological examination of the myocardium was performed . In the myocardium , the relative expression levels of NF- kB , miRNA-21, miRNA-133, and miRNA-203 were determined . RESULTS. After 4 months in rats with NE on a standard diet , an increase in blood pressure , an increase in the mass index of the LV myocardium was recorded . MBD with the inclusion of 10% Ketosteril slowed down the growth of systolic blood pressure and the development of LV myocardial hypertrophy in rats with kidney dysfunction . At the histological level , the use of LPD provided a decrease in the degree of hypertrophy of cardiomyocytes and degenerative changes in cardiomyocytes . Animals treated with LPD had less pronounced diffuse and perivascular fibrosis compared with animals fed normal food . The use of MBD slowed down the increase in the relative level of expression of the NFκB gene and miRNA-21 in the myocardium of rats with NE and promoted an increase in the expression level of miRNA-133 and miRNA-203 compared to the indices of animals with NE that received standard food . CONCLUSION: long-term use of LPD with the use of ketoanalogues of essential amino acids can have a potential cardioprotective effect in CKD, slowing down the growth of blood pressure , an increase in LV myocardial mass and the formation of structural changes in the myocardium . It is possible that a decrease in the expression of NF- kB and miRNA-21, as well as an increase in the expression of miRNA-203 and 133 in the myocardium , can play a significant role in this .

The problem of studying the functional reserve of the kidneys attracted the attention of nephrologists about 40 years ago. However, to date, a single protocol for performing functional load tests has not been developed. When assessing the excretory function of the kidneys, nephrologists, as before, are guided by the value of the glomerular filtration rate. However, in two patients of the same age and gender, the same value of this indicator cannot be interpreted unambiguously. In this article, we consider the technical features of performing load tests using egg white, "red meat", a mixture of amino acids, 0.5 % sodium chloride solution. All of them require time and labor resources. This limits the possibilities of their use in outpatient settings. We believe that it is necessary to determine the functional reserve in patients without primary kidney pathology, that is, persons with an established diagnosis of diabetes mellitus or hypertension with a disease duration of at least 5 years. Serious nephroprotective measures in them are recommended to begin only at the stage of chronic kidney disease C3a. It is possible that such a late start of secondary prevention partly explains the increase in the proportion of such patients in hemodialysis centers.

INTRODUCTION. A high intake of sodium chloride from food is associated with damage not only to the cardiovascular system but also to the kidneys. The mechanisms of the negative effects of high-salt diets on the kidneys have not been established. One of the important links in this process can be microRNAs, which can modulate gene expression at the post-transcriptional level. It is also not known whether soy proteins can counter the kidney remodeling associated with increased salt intake.THE AIM. To estimate the expression levels of miRNA-133 and 203 in blood serum and urine and miRNA-21 in the urine of cynomolgus macaques received diets for a long time with various table salt contents, including and not including soy proteins.MATERIALS AND METHODS. Three groups (6 individuals in each) of male cynomolgus macaques at the age of 6–8 years were studied. The first group (control) received a standard diet, the second – a diet with a high content of table salt (8 g NaCl / kg feed), the third – a diet with high salt content in combination with SUPRO 760 soy protein (200 g protein/kg feed). Blood pressure was measured in animals 12 months later. In monkey urine, the relative expression levels of miRNA-21, miRNA-133, and miRNA-203 were determined, in blood serum – the expression levels of miRNA-133 and miRNA-203.RESULTS. During the follow-up period in the control group, there were no significant changes in the studied parameters. In the groups that received high-salt diets throughout the year, blood pressure also did not change significantly. There was no change in the level of expression of miRNA-133 in the blood serum of monkeys fed a high-salt diet and a standard protein diet. However, in macaques fed a diet high in salt in combination with soy protein, the serum expression of this miRNA was significantly reduced. The expression of miRNA-203 in blood serum did not change significantly. In the control group, there were no changes in the expression of miRNA-21 in urine. In the other two samples, this parameter increased in comparison with the initial values. Both high-salt diets resulted in a significant increase in the relative level of miRNA-133 expression in urine compared to basal values. However, the increase in this indicator in the group of animals fed a high-salt diet in combination with soy isolate was significantly less than in monkeys fed only a high-salt diet. Expression of miRNA-203 in urine was significantly increased only in the group with a high content of table salt without added soy protein.CONCLUSIONS. It is possible that the effects of high-salt diets on the kidney may be mediated by epigenomic mechanisms and partially modulated by the inclusion of isolated soy proteins in the diet.

High food intake of sodium chloride is associated with damage not only the cardiovascular system, but also the kidneys. The mechanisms of the potential negative effects of high-salt diets on the kidneys have not been established. The aim of the study was to trace the changes in relative expression of miRNA-21, 203 and 133 in urine of cynomolgus macaques (Macaca fascicularis) fed high-salt diet with and without isolated soy proteins. Material and methods. The object of the study was 18 male cynomolgus macaques (Macaca fascicularis) aged 6-8 years with a body weight of 5.1-9.7 kg. The animals were divided in 3 groups (6 individuals each). The animals of the first (control) group received a standard diet (2 g NaCl/kg feed). The animals of the second group were fed high-salt diet (8 g NaCl/kg feed), of the third - high-salt diet combined with SUPRO 760 isolated soy protein (200 g/kg feed; instead of milk and egg proteins, corn gluten). Access to water was free. The follow-up period in this study was 4 months. In animals blood pressure (BP) and relative level of microRNA (miRNA) expression in urine were measured. Results and discussion. Keeping monkeys on the studied diets for 4 months did not lead to significant changes in systolic or diastolic BP compared with the initial level. In the control group, there were no distinct changes in the expression of miRNA-21 in urine during observation. In the other two groups, there was a significant increase (approximately equally) of this parameter in comparison with the initial values. Both high-salt diets resulted in a significant increase in the relative level of expression of miRNA-133 and miRNA-203 in urine compared to basal values. However, the increase in these parameters in the group of animals fed a high-salt diet in combination with soy isolate was significantly less than in monkeys fed only a high-salt diet. Conclusion. Possible, potentially negative effects of high-salt diets on kidney may be mediated by epigenomic mechanisms and partially modulated by the inclusion of isolated soy proteins in the diet.

Uromodulin (UMO) is a multifunctional glycoprotein expressed in the epithelial cells of the thick ascending part of the loop of Henle. Currently a lot of data about mechanisms of biosynthesis, apical and basolateral transport of UMO, changes in urine and blood concentrations in different kidney compartments damage, roles of UMO in protecting kidneys from infections, maintaining mineral homeostasis, development of arterial hypertension and the participation of this glycoprotein in other physiological and pathological processes has been accumulated. The article discusses the clinical significance of UMO in the development and progression of chronic kidney disease, prognostic value of UMO urine and blood concentrations in terms of the risk of cardiovascular diseases and probability of acute kidney damage in patients with cardiovascular pathology. Briefly highlights issues of UMO gene mutation and development of autosomal dominant tubulointerstitial kidney disease.

INTRODUCTION . High dietary sodium chloride intake has traditionally been considered an important factor in cardiovascular risk and an increase in blood pressure (BP). However, much remains unclear about the relationship between dietary sodium and cardiovascular health. In particular, it was shown that in rats a high content of salt in the diet can lead to miocardial remodeling/damage without increasing BP. It is possible whether this phenomenon in primates remains unknown. The AIM of the study was to trace the dynamics of BP and some echocardiographic (EchoCG) parameters in cynomolgus macaques ( Macaca fascicularis ), which have been on a high sodium chloride diet for a long time. MATERIAL AND METHODS . 12 male cynomolgus macaques 6-8 years with a body weight of 5,15-9,7 kg were studied. The animals were divided into two groups (six individuals each). The first (control) received a standard diet, the second – a diet high in sodium chloride (8 g NaCl/kg feed). After four and fourteen months, in the animals were measured blood pressure and conducted echocardiographic examination (EchoCG). RESULTS . During the follow-up period in the control group, no significant changes in the studied parameters were recorded. Increased salt intake at four months resulted in a significant decrease in left ventricular end-systolic dimension and an increase in ejection fraction values. After fourteen months, both of these indices returned, practically, to the initial level, but there was a significant increase in the thickness of the posterior wall of the left ventricle in systole and a decrease in systolic excursion of the tricuspid valve annulus compared with the basal data. BP in the salt group also did not change significantly. CONCLUSION . Cynomolgus macaques are able to resist an increase in blood pressure induced by a long stay on a high-salt diet, but in primates under such conditions, the initial manifestations of functional and structural rearrangement of the heart can be observed.

Background. Even a moderate decrease in glomerular filtration rate leads to an increased risk of cardiovascular diseases (CVD), which is the leading cause of mortality in patients with chronic kidney disease (CKD). Left ventricular hypertrophy (LVH) underlies CVD development in renal dysfunction. The prevalence of LVH in patients with CKD stages 2–4 is 50–70 % and reaches 95 % at the beginning of dialysis, which significantly exceeds the number of cases in general population (15–21 %). Common hemodynamic factors associated with chronic kidney damage —hypertension (HTN), activation of the renin-angiotensin system, anemia, fluid and sodium retention, and others largely explain the high prevalence of LVH among patients with CKD. Nevertheless, the existence of additional non-hemodynamic mechanisms of myocardial remodeling (MR) is evident.Objective. To investigate the associations between the MR physiological/histological characteristics and laboratory parameters of calcium-phosphate metabolism in the initial stages of experimental CKD. Design and methods. Four groups of spontaneously hypertensive rats (SHR) were studied (n = 35): 3/4 nephrectomized rats (Nx) one month exposed after surgery (Nx(1), n = 9), 5/6 Nx two months after surgery (Nx(2), n = 8), sham operated rats one month after surgery (SO(1), n = 9) and two months after surgery (SO(2), n = 9). Myocardial mass index (MMI), systolic blood pressure (BP), proteinuria, creatinine (Cr) concentration, total calcium (Ca) and inorganic phosphate (Pi), 25-OH vitamin D (25OHD) and parathyroid hormone (PTH) in serum, myocardial morphology were studied in all experimental animals.Results. The models corresponded to the 1–3 stages CKD. There were no significant changes in serum total Ca (p = 0,066), Pi (p = 0,051) and PTH (p = 0,015) concentrations, the level of 25OHD was significantly lower in Nx(2) rats vs control (p = 0,015). MMI increased in all nephrectomized rats (p = 0,008). The cardiomyocytes (CM) thickness increased in Nx(1) and Nx(2) animals compared to the corresponding controls (p = 0,010, p = 0,002). A significant increase in interstitial (IF) and perivascular (PF) fibrosis occurred in Nx(2) rats with more damaging influence (p = 0,017, p = 0,004). CM thickness, IF and PF increased with the elevation of BP (r = 0,39, p = 0,038, r = 0,47, p = 0,026, r = 0,49, p = 0,031) and serum Cr (r = 0,68, p = 0,001, r = 0,61, p = 0,003, r = 0,69, p = 0,001), and the decrease in serum 25OHD concentration (r = –0,045, p = 0,047, r = –0,50, p = 0,020, r = –0,52, p = 0,012). Multiple linear regression analysis showed, that 25OHD is an independent predictor of myocardial fibrosis (IF: β = –0,38 ± 0,18, p = 0,047, PF: β = –0,34 ± 0,15, p = 0,032).Conclusions. The initial stages of CKD accompanied with HTN are associated with serum 25OHD concentration decrease CM hypertrophy and myocardial fibrosis. The CM growth is an earlier event in relation to the interstitial fibrosis. The obtained data suggest a possible role of vitamin D deficiency in the development of myocardial fibrotic lesions.

INTRODUCTION . From 15 to 35% of cases of acute coronary syndrome (ACS) are complicated by the development of acute kidney injury (AKI), prevention and early intervention remain the most effective strategy for managing patients with AKI in ACS. THE AIM: This study aimed to explore a risk factors and biomarkers for predictive and early diagnostic of AKI in ACS. PATIENTS AND METHODS . The study included patients hospitalized with a diagnosis of ACS in Pavlov First Saint Petersburg State Medical University. In case of exclusion of ACS, patients were determined in the comparison group, in case of confirmation of the diagnosis of ACS – in the study group. Biomaterial (blood) was taken at admission (T1), 1 day after admission (T2) and 2 days after admission (T3). For the diagnosis of AKI, KDIGO 2012 criteria were used. The measured biomarkers at each point were sST2, troponin I, NTproBNP. RESULTS . The study included 132 patients, the diagnosis of ACS was confirmed in 91 patients and AKI development was in 30 patients, all from the ACS group. The most significant for predictive diagnosis was the assessment of GRACE score> 133 points (AUC=0.760, p=0.001), sST2 level> 27.2 ng / ml (AUC=0.737, p=0.001), Mehran score> 5 (AUC=0.916, p=0.001), modification of the Mehran score (adding 2 points if the patient has sST2> 27.2) increases the predictive ability of AKI, Mehran+sST2> 7 points – AUC=0.928, p=0.001. CONCLUSIONS . The use of a combination of clinical data (hemodynamic parameters, presence of heart failure, routine laboratory data, presence of AKI risk factors) and assessment of biomarkers level, in particular the sST2 level, seems to be an effective method for predictive diagnosis of AKI and requires further research.

BACKGROUND. Increased salt intake is associated with a number of cardiovascular events, including increased blood pressure (BP) and the development of left ventricular hypertrophy (LVH). However, there is much evidence that a high content of sodium chloride in the diet does not always lead to an increase in BP, but almost inevitably causes cardiac remodeling, in particular, LVH. Many aspects of myocardial remodeling induced by high sodium content in the food have not been studied enough. THE AIM of the study was to trace the echocardiographic changes in Wistar rats fed the high salt ration and the high salt ration supplemented with soy proteins.MATERIAL AND METHODS. Echocardiography and BP measurements were performed on male Wistar rats, divided into three groups. The first (control; n = 8) included rats that received standard laboratory feed (20.16 % animal protein and 0.34 % NaCl); the second (n = 10) – animals that received standard feed and 8 % NaCl (high salt ration). The third group (n = 10) consisted of rats who consumed a low-protein diet containing 10 % soy protein isolate (SUPRO 760) and 8 % NaCl. The follow-up period was 2 and 4 months.THE RESULTS of the study showed that: (1) the intake of a large amount of salt with a diet does not necessarily lead to the formation of arterial hypertension; (2) despite the absence of a distinct increase in BP, under these conditions signs of cardiac remodeling, in particular, LVH, appear rather quickly; (3) supplementing a high-salt diet with soy isolates counteracts the development of LVH.CONCLUSION. High salt intake with food can cause heart remodeling, regardless of blood pressure, while soy proteins can counteract this process.

Background and objective.Currently, the role of miRNA‑21 in the development of heart and kidney damage and their interaction remains unclear. Therefore, the aim of this work is to assess the impact of changes in the expression of microRNA‑21 in myocardial tissue in the development of cardiac remodeling with chronic reduction in the mass of active nephrons in the experiment.Design and methods.Wistar drain rats were divided into two groups. The first (control) group included nine falsely operated animals. The second (n = 9) group included rats with step-by-step resection of 5/6 renal tissue. After 4 months after surgery, blood pressure (BP) was measured, heart ultrasound (echocardiography, EchoCG) was performed and the level of relative expression of microRNA‑21 in myocardial tissue was determined.Results. The rats with an experimental decrease in the mass of functioning nephrons, showed significantly higher levels of BP, microRNA‑21 expression in the myocardium and the thickness of the interventricular septum (according to EchoCG). They also demonstrated smaller end-systolic dimension of the left ventricle and systolic motion of the mitral valve ring.Conclusions. Our data indicate the potential role of miRNA‑21 in the development of concentric left ventricular remodeling while reducing the number of functioning nephrons. This remodeling is characterized by the prevalence of myocardial hypertrophy over fibrosis. However, the specific mechanisms linking microRNA in the pathogenesis of heart remodeling require further research.

INTRODUCTION. Acute Kidney Injury (AKI) is a common complication of acute coronary syndromes (ACS), and associated with higher mortality and adverse outcomes. Despite advances in research over the past years, effective treatments for current AKI are not available. Prevention and early intervention remain the most effective strategies for AKI of any entity. THE AIM: This study aimed to explore a risk factors and biomarkers for predictive and early diagnostic of AKI in ACS.PATIENTS AND METHODS. Study was prospective and cohort, patients hospitalized with ACS in Pavlov First Saint Petersburg State Medical University were included. In case of exclusion of ACS, patients were determined in the comparison group, in case of confirmation of the diagnosis of ACS – in the study group. Biomaterial (blood and urine) was taken at admission (T1), 1 day after admission (T2) and 2 days after admission (T3). For the diagnosis of AKI, KDIGO 2012 criteria were used. The measured biomarkers at each point were NGAL, KIM-1, cystatin C, sST2, troponin I. RESULTS. The study included 73 patients, the diagnosis of ACS was confirmed in 40 patients and AKI development was in 15 patients, all from the ACS group. The most significant for predictive diagnosis was the assessment of the parameters of systemic hemodynamics and the severity of acute heart failure (AHF): heart rate>89 (AUC=0,798, p=0,001), GRACE Risk Score>133 (AUC=0,926, p=0,005). In evaluation the suitability of biomarkers in terms of prognostic diagnosis of AKI, urine NGAL>32 ng/ml (AUC=0,814 p=0,04) and sST2>23.4 ng/ml (AUC=0,718, p=0,02) showed the best results.CONCLUSIONS. In study of biomarkers efficiency, the use of urine sST2 and NGAL is most promising. Together with hemodynamic parameters, biomarkers have high predictive ability in the diagnosis of AKI in ACS.

Aging causes significant changes in the kidneys. One of the most important manifestations of an aging kidney is a reduction in glomerular filtration rate (GFR). Unfortunately, there is no generally accepted, adequate method for evaluating GFR in the elderly. The perspectivies of the relatively new approaches (BIS1, BIS2, FAS) are not clear and doubtful. The feasibility of standardization of GFR values by body surface area among of the older persons has not been determined. Possible that the diagnosis setting «chronic kidney disease» in elderly solely on the base of GFR decline may be an inadequate approach and promote a kind of «nephrological ageism».

The aim: to evaluate the effect of the sodium-glucose cotransporter SGLT-2 inhibitor – empagliflozin on the kidney in nondiabetic Wistar rats with experimental heart failure (HF). Material and methods . Chronic HF was induced by ligation the left coronary artery. Animals with HF in the first group (n=11) received empagliflozin (Jardiance®, Boehringer Ingelheim) orally (1 mg / kg/day) for 1 month. In the second group of rats with HF (n = 10) the drug is not administered. Concentrations and daily urinary excretion of glucose, protein and albumin were measured. The relative level of microRNA-21 urinary expression was established. Morphological examination of kidney tissue was performed using light microscopy. Results. The administration of empagliflozin to experimental animals resulted in regularly higher values of diuresis, glucose concentration in urine and its daily excretion. There were no significant differences in levels of albuminuria and proteinuria or miRNA-21 expression in urine in groups with and without empagliflozin. The animals receiving the drug showed a slightly less pronounced damage to the cells of the tubular epithelium compared to rats with only heart failure. Conclusion. The data obtained, at least confirm the renal safety of long-term empagliflozin administration even under conditions of high risk.

In 2002 a group of experts Acute Dialysis Quality Initiative (ADQI) developed a definition of acute renal kidney failure (ARF) and created a system of its risk stratification. (RIFLE-criteria). In 2004 was proposed a conception of «acute injury» (AKI), and in 2007 an experimental group Acute Kidney Injury Network (AKIN) offered a diagnostic criteria system and evaluation of the degree of such condition (AKIN-criteria), which was a modification of RIFLE classification system. Both systems gave a good showing of themselves in practice for the prediction of the development of AKI and its outcome in patients in critical condition. However, not the RIFLE system, nor the AKIN system initially did not suppose to include the patients with acute primary parenchymatous renal damage, which does not satisfy the nephrological community. A modification of the AKIN system, which allows to dismiss such limitation, was proposed.

THE AIM of the study. Clarify the meaning of interleukin-6 in the pathogenesis of «uremic malnutrition» in patients with end-stage renal disease (ERSD) receiving chronic hemodialysis (HD). PATIENTS AND METHODS . We examined 86 patients with chronic kidney disease stage V receiving HD treatment, including 40 women and 46 men aged 52.2 ± 1.3 years. The cause of TRD in all cases was primary glomerulonephritis. All patients received hemodialysis treatment program for 6,4 ± 1,1 years. To estimate the daily intake of protein, fats, carbohydrates, total caloric intake, patients filled out food diaries for a week. To assess the nutritional status using kaliperometry and integrated dual frequency impedansometry using an instrument KM - AR - 01 firm «Diamond», Russia. In 78 patients to determine the spectrum of pro-inflammatory cytokines - interleukins - 2, 6, 8, granulocyte-macrophage colony-stimulating factor (GM-CSF), interferon gamma (IFN-g), TNF-αwith the help of Human 8-plex A panel (171-A11080 ) company Bio-rad, USA, a method based on the selective binding of defined cytokines and sorbed on the surface of micro particle antibodies. RESULTS . The interrelation between increased levels of interleukin-6 and «uremic malnutrition» in patients with end-stage renal failure receiving chronic hemodialysis was detected. Was shown that the increase of the duration of hemodialysis therapy was accompanied by increased signs of chronic inflammation. CONCLUSION . Increased IL-6 serum may be one of pathogenetic factors involved in the development of «uremic malnutrition» in patients with end-stage renal failure receiving chronic hemodialysis.