Introduction. Rapid and reliable assessment of circulating antibody levels to SARS-CoV-2 remains the current challenge for monitoring and preventing the spread of COVID-19. As the risk of emergence and dissemination of new viral strains continues to grow, epidemiologic research is also becomes increasingly important. The enzyme-linked immunosorbent assay (ELISA) is useful to assess the vaccination effectiveness and the need for revaccination, the proportion of post-disease and vaccinated individuals, and to monitor population immunity. This article provides an overview of the local ELISA kits currently available for the detection of antibodies against SARS-CoV-2 viral proteins, with a comparison to the certified kit by Mediagnost Ltd. (Germany).The aim. Laboratory testing of seven domestic reagent kits for the determination of antibodies to SARS-CoV-2 viral proteins by ELISA in comparison with the certified test system “Anti-SARS-CoV-2 ELISA E 111-IVD” (Mediagnost Ltd., Reutlingen, Germany).Materials and methods. The study included 80 serum samples from conditionally healthy donors: experimental group (n=70, serum samples collected after 2019) and control group (n=10, serum samples collected before 2018). The experimental group is comprised of non-infected and post-disease individuals; a proportion of those were vaccinated against COVID-19.Results and conclusions. The data obtained indicate high reproducibility, sensitivity (100 %), and specificity for all domestic ELISA kits in detecting both post-disease (90–95 %) and vaccinated volunteers (100 %). The main quality criteria of the obtained results were comparable to those for the certified test system, “Anti-SARS-CoV-2 ELISA E 111-IVD” (Mediagnost Ltd., Germany). All kits detecting IgG to the receptor-binding domain (RBD) and to the S-glycoprotein were effective for the reliable assessment of antibody production after the vaccination. Kits for the detection of antibodies to the RBD and/or viral nucleocapsid are useful for identifying unvaccinated post-disease individuals.

End-stage renal disease (ESRD) is associated with a variety of erythron alterations including structural and functional changes in circulating erythrocytes (RBCs), which are potential risk factors to cause RBC malfunctions and corresponding anemia of different severity. However, the mechanisms of such changes in RBCs remain understudied. Here we used flow cytometry to estimate intracellular esterase activity, phosphatidylserine externalization, and reticulocyte count and state, laser diffraction for osmotic and ammonium stress tests, and spectrophotometry to evaluate the generation of unstable hemoglobin (Hb) forms in RBCs of patients with ESRD before and after the hemodialysis (HD) session. RBCs in ESRD were more osmotically fragile and had an increased swelling rate in the ammonium stress test. HD did not affect RBC deformability but led to Hb oxidation to ferryl forms and triggered such apoptosis-like events, as a decrease in intracellular esterase activity and an increase in the number of annexin-V-positive cells. Our data indicate that uremic syndrome, combined with the mechanical and chemical effects of HD therapy, challenges the erythron of HD patients and contributes to a multifactorial decrease in RBC function and aggravation of renal anemia.

End-stage renal disease (ESRD) is associated with a range of erythrone alterations, such as structural and functional changes of circulating erythrocytes, which are the potential risk factors to cause erythrocyte malfunctions and corresponding anemia of different severity; however, the mechanisms of such changes in erythrocytes remain understudied. Here we used flow cytometry for estimation of the changes in intracellular esterase activity, phosphatidylserine externalization, and reticulocyte count and state; laser diffraction for osmotic and ammonium stress tests, and spectrophotometry for oxidized hemoglobin evaluation in erythrocytes of patients with ESRD before and after the hemodialysis (HD) session. Erythrocytes of ESRD patients were more osmotically fragile and had increased swelling rate in ammonium stress test. HD did not affect erythrocyte deformability but lead to hemoglobin oxidation to ferryl forms and triggered apoptosis-like events, such as a decrease in the intracellular esterase activity and increase in the number of annexin-positive cells. Our data indicate that uremic syndrome, combined with the mechanical effects of the HD system, challenges the erythron of HD patients and contributes to a multifactorial decrease in erythrocyte function and aggravation of renal anemia.

INTRODUCTION . Beta-catenin is a structural protein of adhering junction and intercalated discs of cardiomyocytes as well as the main intracellular messenger of the canonical WNT (cWNT) signaling pathway. The dysregulation of the cWNT signaling and the rearrangement of the cardiomyocyte cytoskeleton accompany the cardiovascular disorders in chronic kidney disease (CKD). THE AIM : to investigate the expression and distribution of β-catenin, calcineurin A, and TGF-β1 in the myocardium of spontaneously hypertensive rats (SHR) with CKD, sham operated SHR and Wistar Kyoto rats of the corresponding age. MATERIAL AND METHODS . Systolic blood pressure (BP), heart rate (HR), myocardial mass index (MMI), creatinine concentration (Cr), myocardial beta-catenin expression and renal Klotho expression, morphological light-optical study of kidney and myocardium tissues was performed in sham operated (SO) Wistar Kyoto rats (WKY), spontaneously hypertensive rats (SHR) and SHR with 5/6 nephrectomy (Nx). RESULTS . SHR rats showed higher values of BP, MMI, cardiomyocyte diameter, myocardial fibrosis area, and lower Klotho levels compared to WKY rats. Nx SHR had lower kidney function and renal Klotho expression, higher BP and MMI compared to SHR. An increase in the cardiomyocytes diameter and the area of myocardial fibrosis was accompanied by the overexpression of β-catenin, calcineurin A, and TGF-β1 in the myocardium. CONCLUSION . The upregulation of canonical Wnt signaling and cellular programs of cardiomyocyte hypertrophy mediated by Klotho deficiency can be involved in myocardial remodeling in chronic renal dysfunction.

THE AIM . Comparison of indirect immunofluorescence (IIFT) and enzyme-linked immunosorbent assay (ELISA) methods for the determination of circulating antibodies to the podocytic transmembrane receptor of M-type secreted phospholipase A 2 (PLA 2 R-AB) in patients with primary membranous nephropathy (PMN). PATIENTS AND METHODS . The study included 54 patients with PMN (M: F [33:21]) aged 55 (40-63) years and 10 apparently healthy individuals of the corresponding gender and age. Proteinuria and glomerular filtration rate (eGFR) was determined in all patients. The anti-PLA 2 R-AB levels were measured by indirect immunofluorescence (IIFT) and enzyme-linked immunosorbent assay (ELISA) using EURUIMMUN AG test systems (Lubeck, Germany). RESULTS . The levels of anti-PLA 2 R-АB determined by the two investigated methods were changed in the same direction (r = 0.82, p < 0.005). The ELISA method made it possible to detect a larger number of anti-PLA 2 R-positive cases, both in the group of patients before treatment (ELISA – up to 80 %, IIFT – up to 67 %) and among patients receiving immunosuppressive therapy (ELISA – up to 63 %, IIFT – up to 50 %). The concentration of autoantibodies determined by ELISA (both quantitative and semi- quantitative) correlated with proteinuria (r = 0.69, p = 0.001) and eGFR (r = -0.38, p = 0.035). The response to therapy was more clearly traced when the study was performed by quantitative ELISA. CONCLUSION . The ELISA method is more effective in identifying PLA 2 R-positive patients with PMN, allows obtaining quantitative results and assessing the dynamics of the concentration of autoantibodies, which contributes to the early correction of the therapy and decisionmaking on immunosuppressive treatment.

Introduction . The key point of cardiorenal relationships is the activation of the renin-angiotensin-aldosterone system and the formation of endothelial dysfunction. The aim of our study was to assess the state of endothelium-dependent vasodilation (EDVD) in patients with chronic kidney disease (CKD) as a function of the glomerular filtration rate (GFR). Materials and methods . It was investigated 40 healthy men (mean age 39.2±2.0 years) and 72 patients with CKD I st. (mean age 42.5±11.9 years). GFR was calculated using the formula CKDEPI. Tissue perfusion was studied by high-frequency ultrasound Doppler. Vascular reactivity of the skin was evaluated in functional tests with ionophoresis of acetylcholine. Results . Compared with healthy individuals, the increase in the volumetric blood flow velocity at the 2 minute test with acetylcholine was reduced only at a GFR value of 90–109 ml/min/1.73 m 2 , with large values of GFR, no indicator changes were detected. Also, only in these patients the most significant violations of oxidative status were noted in the form of an increase in the concentration of diene conjugates in the blood serum, a decrease in the concentration of tocopherol and general SH groups. Conclusions . Disturbance of endothelium-dependent vasodilation in the sample with acetylcholine in patients with the first stage of CKD was established with a GFR value of less than 109 ml/min/1.73 m 2 . Disturbance of the indicators of oxidative status was noted with a GFR value of less than 109 ml/min/1.73 m 2 .

Glomerular filtration rate (GFR) is a recognized indicator of the functional status of the kidneys. In medical practice, there are various approaches for measuring GFR. However, despite the nearly 100-year history, not all methodological problems of evaluating GFR in clinical practice have been solved. The most physiologically justified (“reference”) methods are not acceptable in routine practice because of the complexity and high cost. Therefore, clinicians have to rely mainly on the results of surrogate methods, most of which use endogenous creatinine as a glomerulotropic test agent. Therefore, the accuracy of determining the concentration of this metabolite in biological media (especially in serum) is often crucially determined by the reliability of the GFR assessment. Manufacturers of creatinine reagent kits should take into account current requirements for accuracy and traceability of measurement results and ensure that their products comply with international standards.

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. Klotho is a transmembrane and circulating protein primarily synthesized by the kidney. Klotho deficiency characterizes chronic kidney disease (CKD), as myocardial hypertrophy (GM). The cardioprotective effect of the Klotho protein is due to the negative regulation of a variety of stress signals, leading to the activation of the hypertrophic intracellular signaling pathway calcineurin (CaN) / NFAT in the myocardium. The effect of Klotho may presumably be mediated by the modulation of Ca2 + channels and / or Foxo factors essential for CaN signaling. THE AIM: to study the activity of CaN/ NFAT signaling pathway in the myocardium and to determine the molecular mechanisms of its regulation in conditions of Klotho level decrease in spontaneous hypertensive rats (SHR) with experimental CKD. MATERIAL AND METHODS. The experimental model of CKD was 3/4 or 5/6 nephrectomy (Nx) in SHR. Sham-operated (SO) SHR, and Wistar Kyoto rats (WKY) were used as controls. In all animals were measured systolic blood pressure, myocardial mass index – MMI, creatinine clearance, cardiomyocyte (CM) diameter, Klotho levels in serum (ELISA) and kidney (IHC), myocardial expression of calcineurin (IHC, PCR), transcription factor NFAT (IHC), TRPC6 (IHC), FOXO3A (PCR) and phosphor-Foxo1/3/4 (IHC). The tissue expressions of calcineurin, TRPC6, and Klotho were calculated as the IHC specific product area to the field of view ratio. NFAT expression was evaluated as the positively stained nuclei to the number of nuclei ratio in the field of view. Measurements were performed in 10 fields of view for each histology slide. RESULTS. The model has corresponded to the initial stages of CKD. The increase in MMI (p = 0.005) and CM diameter (p = 0.002) were observed compared in Nx rats to SO. Renal Klotho expression (p < 0.001), and serum Klotho level (p = 0.019) were lower in the Nx. In multiple linear regression analyzes, the values of MMI and CM thickness were independently associated with the level of renal Klotho protein (β = -0.38 ± 0.16, p = 0.026, β = -0.64 ± 0.14, p <0.001, respectively). Nx and systemic hypertension were accompanied by an increase in the expression of the calcineurin gene (p = 0.005) and cytoplasmic calcineurin in CM (p = 0.004), the number of NFAT-positive nuclei (p = 0.007), and an increase in the expression of the FOXO3A gene (p <0.001) in the absence of accumulation of phosphorylated Foxo1/3/4 in CM cytoplasm. SHR rats were characterized by positive IHC staining for TRPC6 compared to WKY (p = 0.004). The expression of calcineurin and TRPC6 varied co-directionally (r = 0.69, p <0.001), and both of these indicators were associated with the Klotho levels (calcineurin vs Klotho in the kidney, r = -0.73, p <0.001; TRPC6 vs Klotho in serum, r = -0.43, p = 0.025). CONCLUSION. The development of Klotho deficiency on early-stage CKD is associated with the expression of transient Ca2+ channels TRPC6 and activation of the calcineurin / NFAT hypertrophic signaling pathway in cardiomyocytes.

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.

BACKGROUND. The molecular mechanisms of the initial stages of inorganic phosphate (Pi) metabolic disorders in chronic kidney disease (CKD) remain poorly understood.THE AIM. To test the hypothesis about changes in canonical Wnt signaling pathway inhibitors biosynthesis and a concomitant decrease in bone turnover as one of early mechanisms of Pi imbalance in CKD.MATERIAL AND METHODS. Creatinine (Cr), inorganic phosphate (Pi), serum parathyroid hormone (PTH), fibroblast growth factor 23 (FGF23), osteoprotegerin (OPG), sclerostin (SOST) and Dickkopf-1 (DKK), renal SOST and DKK mRNA expression, albuminuria (Alb), proteinuria (uTP) levels, fractional (FEPi) and daily (uPi24) Pi excretion were analyzed in SHR rats (N = 52) with 3/4 nephrectomy (NE) or sham operation (SO) and observation periods of 2, 4, and 6 months.RESULTS. Experimental model was comparable with 1-2 stages of CKD. In groups NE4 and NE6, the concentration of sPi and renal Pi excretion (FEPi and uPi24) were significantly higher vs corresponding controls SO4 (p = 0.006, p <0.010) and SO6 (p = 0.002, p = 0.028). Serum concentrations of FGF23 and PTH in NE and SO animals did not change significantly. In NE4 and NE6 groups, serum SOST and DKK concentrations were significantly higher vs controls (p <0.049, p <0.043), while the kidney expression SOST and DKK mRNA in NE rats did not change significantly or decreased (p = 0.002, p <0.011). The serum concentration of OPG was higher in the NE6 vs SO6 control (p = 0.028).CONCLUSION. The initial stages of experimental CKD are characterized by an increase in serum concentrations of Dikkopf-1, sclerostin and osteoprotegerin. The obtained data suggest the possible role of canonical Wnt signaling inhibition and reduction of bone turnover in the pathogenesis of Pi metabolic disorders in early stages of CKD.

INTRODUCTION. Vitamin D deficiency is commonly observed in patients with chronic kidney disease (CKD) due to decreased biosynthesis of 1,25(OH)2D3 in damaged renal tubules and increased catabolism of 1,25(OH)2D3 and 25OHD3. There is a growing evidence that vitamin D deficiency may contribute to impaired kidney function. Interventional studies have shown that vitamin D and its analogs attenuate the progression of renal fibrosis in experiment, and reduce proteinuria in patients with CKD. The renoprotective effects of vitamin D go far beyond its classical role in maintaining bone and mineral metabolism, which is a result of its pleiotropic action. THE AIM: to investigate the association between 25OH-hydroxyvitamin D (25OHD) level and renal fibrosis in spontaneously hypertensive rats (SHR) with early stages of experimental CKD.MATERIAL AND METHODS. Systolic blood pressure (BP), proteinuria, albuminuria, creatinine (Cr), urea (Ur), inorganic phosphate (Pi), 25OHD in serum were measured in nephrectomized (NE) and sham operated (SO) spontaneously hypertensive rats SHR (follow-up period 2, 4 and 6 months) and SO Wistar Kyoto rats (follow-up period 2 months), morphological light-optical study of kidney tissue was performed.RESULTS. The experimental model corresponded to the initial stages of CKD (Ur: 6.64 – 13.36 mmol/L). A significant increase in the area of renal fibrosis in animals with NE correlated with an increase in blood pressure (r = 0.51, p <0.001), serum Cr (r = 0.76, p <0.001), and albuminuria (r = 0.64, p <0.001) and proteinuria (r = 0.78, p <0.001) and a decrease in the concentration of 25OHD in serum (r = -0.67, p <0.001). In multiple regression analyzes, a reliable association of fibrosis with 25OHD was maintained (β = -0.28, p = 0.012). In addition, in ROC-analysis the largest value of the area under the curve was obtained for 25OHD (AUC = 0.95) to detect interstitial fibrosis more than 10 %.CONCLUSION. 25OHD depression at the initial stages of experimental CKD and hypertension is independently associated with the development of renal fibrosis.

INTRODUCTION.It is suggested that fibroblast growth factor 23 (FGF23) and its co-receptor Klotho are probably associatedwith changes in calcium metabolism in chronic kidney disease (CKD) due to ability to regulate intracellular Ca transport bymodulating the cationic channels TRPV5 and TRPV6.THE AIMis to investigate the association between Klotho, FGF23 and renal excretion of Ca in the initial stages of experimental CKD.MATERIAL AND METHODS.The experimental models of chronic kidney injury were resection of the renal tissue in spontaneously hypertensive rats (SHR). Serum concentrations of intact FGF23 and PTH were determined by ELISA, renal Klotho protein expression by IHC. The indices of Ca excretion were calculated.RESULTS.Serum creatinine concentration, creatinine clearance and the severity of interstitial fibrosis in experimental models corresponded to the initial stages of chronic kidney disease. UCa24 and FECa were higher, Klotho protein expression was lower in groups with more severe renal dysfunction, without significant differences in FGF23 and PTH levels. Multiple regression analysis showed that FECa and UCa24 were not associated with FGF23, Klotho, and PTH.CONCLUSION.Renal excretion of Ca in initial stages of experimental kidney damage is not associated with Klotho and FGF23 levels.

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. Cronic heart failure (CHF) was induced by ligation the left coronary artery. Animals with CHF 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 CHF (n = 10) the drug is not administered. Systolic blood pressure, heart rate, concentrations and daily urinary excretion of glucose, albumin, creatinine, urea and essential ions were measured. The relative level of microRNA-21 urinary expression was established.RESULTS.Empagliflozin administration led to an increase in glycosuria, albuminuria, and the expression of microRNA-21 in urine. However in this conditions inorganic phosphorus excretion decreased. Empagliflozin did not influence on blood pressure, heart rate or levels of investigated substances excretion including sodium.CONCLUSION. The findings suggest that the SGLT-2 inhibitors may have some negative direct effects on the kidneys. However, in diabetes, such effects of these drugs can be masked by powerful nephroprotective actions associated with the ability of SGLT-2 inhibitors to counteract hyperglycemia and glomerular hyperfiltration.

The quantification of specific urinary proteins in high-grade proteinuria can be of importance for the evaluation of mophrological lesions, response to therapy and prognosis. The aim of our study was to analyze whether the urinary excretion of high and low molecular proteins associated with the degree of glomerular, tubulointerstitial and vascular fibrosis. Patients and methods. The study included 97 patients with biopsy proven primary immune glomerulopathies: membranous nephropathy (n =22), minimal change disease (n=13), focal segmental glomerulosclerosis (n =30), IgA nephropathy (n=32). Measurements of total protein, immunoglobulin G (IgG), transferrin (Trf), α1-microglobulin (α1-МG), β2-microglobulin (β2-MG) were performed by nephelometric method in morning urine samples. The results were standardized for urine creatinine (Cr) concentration. Results. There were a correlation between proteinuria and specific proteins: β2-MG (r=0.24, р=0.025), α1-МG (r=0.38, р<0.001), Trf (r=0.78, р<0.001), IgG (r=0.67, р<0.001), as well as the positive correlation between high and low molecular proteins. Low molecular proteins (β2-МG, α1-МG) correlated with global glomerular sclerosis (r=0.28, р=0.010 and r=0.21, р=0.049 respectively) while levels of proteinuria and high molecular weight proteins did not. Urinary excretion β2-microglobulin was also significantly higher in patients with moderate-to-severe tubulointerstitial and vascular fibrotic lesions. Conclusion. β2-microglobulin was suggested to be candidate integrative biomarker of renal fibrosis in primary glomerulopathies.

THE AIM: to determine the optimal time and temperature conditions for storage and transportation of urine samples for lipocalin 2 (uNGAL) level measuring. PATIENTS AND METHODS. Levels of uNGAL analyzed by chemiluminescent microparticle immunoassay (Abbott Laboratories, USA) in first morning void urine of 20 patients hospitalized in the Pavlov First Saint Petersburg State Medical University. Urine was transported to the laboratory in ice (+4 °C) within 15 minutes after collection and stored according to different protocols at the temperature -22 °C, +4 °C and +22 °C from four hours to seven days. RESULTS. Concentration of uNGAL is stable for four hours at room temperature (+22 °C), for two days at +4 °C, and at least one week at -22 °C. UNGAL concentration changes significantly when stored for two days at room temperature and for seven days at +4 °C. CONCLUSION. The stability of urinary NGAL concentration allows long distance transport of biological samples to specialized laboratories whereby the study may become available to a wide range of medical institutions.

В.А. Добронравов1, Е.О. Богданова1, Н.Ю. Семенова5, О.Н. Береснева1, М.М. Парастаева1, О.В. Галкина1, И.М. Зубина1, Е.Е. Зуева3, Г.Т. Иванова1, И.Г. Каюков1, Т.Л. Коваленко3, Л.В. Котенко3, Г.М. Нутфуллина2, В.Г. Сиповский1, В.А. Цинзерлинг4, А.В. Смирнов1 ПОЧЕЧНАЯ ЭКСПРЕССИЯ БЕЛКА αKLOTHO, ФАКТОР РОСТА ФИБРОБЛАСТОВ 23 И ПАРАТИРЕОИДНЫЙ ГОРМОН ПРИ ЭКСПЕРИМЕНТАЛЬНОМ МОДЕЛИРОВАНИИ РАННИХ СТАДИЙ ХРОНИЧЕСКОГО ПОВРЕЖДЕНИЯ ПОЧЕК