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the purpose of this work was to study the correlation between oxidative stress (oS) marker and angiotensin converting enzyme (aCe) activity in patients with chronic kidney disease stages I-II (uncomplicated pyelonephritis). the 32 patients with uncomplicated pyelonephritis and 30 healthy volunteers (women, age -18-40 years) R ecently much attention has been paid to the study of renal function in regulating the homeostasis in the assessment of the role of callicrein-kinin, the renin-angiotensin-aldosterone system and prostaglandins, their role in the development of oxidative stress (OS) in chronic kidney disea se (CKD) [1,2]. It is well known that the activation of the callicrein-kinin and renin-angiotensinaldosterone systems causes the increased secretion of vasoactive peptides, including angiotensin II, bradykinin, renin, and promotes the activation of a wide spectrum of neurohormonal, metabolic, inflammatory and procoagulation reactions, that leads to the increase of reactive oxygen species (ROS) [3][4][5][6].The pathogenetic role of angiotensin-II was proved in the development of nephropathy and hypertension. It plays a direct role in the vasopressor effects, promotes intraglomerular hypertension and is one of the key molecules that trigger oxidative stress and inflammation in the vascular wall. One of the effects of angiotensin II is the activation of nuclear transcription factors that stimulates the expression of cytokines, chemokines, nitric oxide (NO), cyclooxygenase-2, adhesion molecules. Endothelial damage primarily affects the production of NO-synthase (NOS) [1,7].Angiotensin-II is involved in the inflammatory reactions and enhances the proliferation of cells, including renal glomerular mesangial cells, contributing to the progression of fibrosis. Another important factor of disorder of renin-angiotensin system is transforming growth factor β (TGFβ), which stimulates synthesis of the various components of the extracellular matrix degradation and blocks protease inhibitors. In addition, TGF-β stimulates the production of endothelin-1 -a powerful vasoconstric-

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Background The present study aimed (i) to evaluate whether ceftriaxone treatment could affect not only intestinal oxalate-degrading bacteria number but their total activity to degrade oxalate and in uence oxalate homeostasis in rats, (ii) to test the effect of commercially available probiotics and a synbiotic on total fecal oxalate-degrading activity, (iii) and to estimate the ability of synbiotic to restore fecal oxalatedegrading activity and ceftriaxone-induced disruption of oxalate homeostasis in rats.Methods Twenty-eight female Wistar rats (200-300 g) were randomly divided into 4 groups (n = 7). Group 1 was treated with vehicle sterile water (0.1 ml, i.m., 14 days); Group 2 received synbiotic (30 mg/kg, per os, 14 days); Group 3 was treated with ceftriaxone (300 mg/kg, i.m., 7 days); Group 4 was supplemented with ceftriaxone and synbiotic. Oxalate-degrading bacteria number and their total activity, urinary and plasma oxalate concentrations were measured on days 1 and 57 after the treatment withdrawal.Results Ceftriaxone treatment reduced total fecal oxalate-degrading activity independently on oxalatedegrading bacteria number and increased urinary and plasma oxalate concentrations. The synbiotic had a high oxalate-degrading activity vs probiotics and was able to restore fecal oxalate-degrading activity and signi cantly decrease urinary oxalate excretion in antibiotic-treated rats.Conclusion Total fecal oxalate-degrading activity but not oxalate-degrading bacteria number should be thoroughly examined in the future to develop predictive diagnostics methods, targeted prevention and personalized treatment in kidney stone disease. Synbiotic supplementation had a bene cial effect on the total oxalate-degrading activity of gut microbiota, which resulted in decreased UOx excretion in rats.

an excess of free radicals accompanies the development of renal pathologies and causes numerous concomitant complications and syndromes. the most common of these are cardiometabolic syndromes in patients with chronic kidney disease. therefore, the purpose of the study was to determine the activity of paraoxonase-1 and myeloperoxidase, which are associated with indicators of high-density lipoproteins content and oxidative stress in the blood of patients with the chronic stage of kidney disease. the activity of the enzymes, thiobarbiturate-active products concentration and transferrin, ceruloplasmin, thiol compounds content were determined in the blood of patients with chronic kidney disease. the oxidative status was shown to be changed. thus, myeloperoxidase activity, the content of oxidized proteins and the concentration of thiobarbiturate-positive components were increased, while the activity of the antioxidant enzyme paraoxonase-1, the content of transferrin, ceruloplasmin and thiol compounds were decreased. the ratio of myeloperoxidase / paraoxonase-1 activities was progressively increased up to 9-fold, indicating the presence of cardiovascular complications in patients. the data obtained allowed to extend the range of indicators for monitoring the development of cardiometabolic disorders in the progression of chronic kidney disease. k e y w o r d s: oxidative status, paraoxonase-1, myeloperoxidase, chronic kidney disease.

BACKGROUND:A large body of research has investigated the effects of pro-atherogenic lipid profile on cardiovascular diseases (CVD) in peritoneal dialysis (PD) patients. However, there is a general lack of research on the association between atherogenic dyslipidemia and PD technique survival.AIM:The study aimed to define the association between dyslipidemia and PD technique survival.METHODS:It was a prospective single-centre observational study involving 40 outpatients on continuous ambulatory PD treatment for more than 3 months between 2010 and 2016 in a single centre in Ukraine. There were 27 males and 13 females. The mean age of the participants was 49.3 ± 12.2 years. The primary outcome measures were all-cause technique failure.RESULTS:Atherogenic dyslipidemia was identified in 28/40 (70 %) patients and correlated with PD adequacy parameters. During the 36-month- follow-up period technique failure occurred in 2/12 (16.6 %) patients with atherogenic dyslipidemia compared with 12 / 28 (42.9 %) patients without atherogenic dyslipidemia (χ2 = 2.5; p = 0.12). In the univariate Cox regression model, atherogenic dyslipidemia at baseline was significantly associated with a higher risk of all-cause PD technique failure (HR 4.5; 95% CI 1.6 to 12.9; χ2 = 5.5, p = 0.019).CONCLUSION:The presence of atherogenic dyslipidemia was significantly associated with a higher risk of technique failure in PD patients. This is an important issue for future research. Further well-designed clinical trials are needed to determine the impact of dyslipidemia on PD adequacy and technique survival.

Background/Aims: It was hypothesized that oxalate might be strongly involved in atherogenesis and the inflammatory pathway that could result in an increased risk of cardiovascular disease (CVD) in end-stage renal disease (ESRD) patients. Therefore, this study aimed to address two primary research questions: to characterize the lipid profile and the pattern of pro-inflammatory cytokines according to plasma oxalic acid (POx) concentration in ESRD patients; to evaluate the potential role of elevated POx concentration in the development of CVD risk. Methods: A total of 73 participants were enrolled in this prospective, observational cohort pilot study. Among them, there were 50 ESRD patients and 23 healthy volunteers. The lipid profile and the pro-inflammatory cytokines were analyzed according to the distribution of POx concentration into tertiles. After the clinical examination, 29 hemodialysis patients and 21 peritoneal dialysis patients without prevalent CVD were observed for CVD events for 2 years. The Cox regression analysis and a set of different types of sensitivity analyses were used to determine whether elevated POx was associated with an increased risk of CVD. Results: An increasing trend in the atherogenic lipoprotein fractions and the pro-inflammatory markers as well as a linear decrease in high-density lipoprotein was significantly associated with elevated POx. POx concentration ≥ 62.9 µmol/L was significantly associated with CVD events independently of other examined CVD risk factors. Conclusions: This pilot study firstly demonstrated a potential contribution of POx to atherogenesis, inflammation and CVD risk in ESRD patients.

Introduction: End-stage renal disease (ESRD) patients have significant differences in plasma oxalic acid (POx) concentration under the same treatment conditions. Objectives: In the present study, we adopted the method of redoximetric titration with a KMnO4 solution to evaluate the effect of total fecal oxalate-degrading activity (ODA) on oxalate homeostasis in ESRD patients which has never been reported before. Patients and Methods: A total of 56 participants were enrolled in this cross-sectional pilot study, including 24 healthy volunteers (a control reference group) and 32 ESRD patients. Among the ESRD patients, there were 21 hemodialysis (HD) and 11 peritoneal dialysis (PD) patients. Total ODA in fecal samples as well as POx concentration, daily urinary oxalate (UOx) and PD effluent oxalate excretion were determined. Cohen’s d was computed to calculate the effect size using post-hoc analysis. Results: Total ODA in fecal microbiota ranged from -23 to 24%/0.01 g of feces and was statistically higher in healthy volunteers compared with the ESRD patients. The ESRD patients with positive total fecal ODA status had higher UOx excretion level and lower POx concentration compared with the patients with negative total fecal ODA status. Cohen’s d effect size was 1.99 and 1.05, respectively. Total fecal ODA was an independent risk factor associated with POx elevation in the ESRD patients. Conclusion: Our pilot study firstly demonstrated a potential role of total fecal ODA in oxalate homeostasis in ESRD patients. The results might be useful for determining sample size considerations and providing groundwork for future research projects.