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.
<b><i>Background:</i></b> We have hypothesized that the problem of dyslipidemia in peritoneal dialysis (PD) patients lies beyond certain levels of plasma lipoprotein and involves cardiovascular risk, but can also influence the development of chronic intraperitoneal inflammation. <b><i>Objectives:</i></b> The aim of our work was to define whether the association of dyslipidemia with intraperitoneal inflammation really exists and if it could it be used in a prospective cohort of PD patients. <b><i>Patients and Methods:</i></b> We performed a cross-sectional, single-center, pilot study involving 40 nondiabetic PD patients (27 men and 13 women with an average age of 49.3 ± 12.2 years). The median time on PD was 29 (18.5–37) months. The parameters dialysis adequacy, blood lipid profile, and the concentrations of tumor necrosis factor (TNF)-α, monocyte chemoattractant protein (MCP)-1, and interleukin (IL)-10 in peritoneal dialysate effluent (PDE) were determined. Cohen’s <i>d</i> effect size was computed post hoc to determine the differences between groups in the concentrations of pro- and anti-inflammatory mediators. <b><i>Results:</i></b> PD patients with atherogenic dyslipidemia had significantly high levels of MCP-1 compared with dyslipidemia-free patients (Cohen’s <i>d</i> = 1.32). A reduced high-density lipoprotein cholesterol level was associated with a high intraperitoneal production of the proinflammatory mediator TNF-α (<i>p</i> < 0.0001) and anti-inflammatory IL-10 (<i>p</i> < 0.0001). Atherogenic index of plasma was directly correlated with MCP-1 (<i>p</i> < 0.0001) and TNF-α (<i>p</i> < 0.0001). In multiple regression analysis, MCP-1 appeared to predict PD inadequacy (<i>R</i><sup>2</sup> = 0.58; <i>F</i> ratio = 9.4; <i>p</i> = 0.006) independently of age and blood C-reactive protein level. Effect size was 1.38 with α = 0.05, <i>n</i> = 40, and 3 predictors. <b><i>Conclusions:</i></b> Our cross-sectional pilot study first demonstrated a close interaction between the atherogenic lipid profile and a high concentration of MCP-1 in PDE; this might be a prognostic marker for PD inadequacy. The potential significance of our finding is that it provides useful preliminary information necessary for further research into this area.
Abstract. In the present exploratory cross-sectional cohort study, we evaluated whether plasma and urine oxalate concentrations in patients with primary glomerulonephritis depend not only on the glomerular filtration rate but also on the proteinuria level and influence the inflammatory response.
Methods. We enrolled 100 participants, including 76 patients with glomerulonephritis having chronic kidney disease stage (CKD) 1–3b (69.7% of them with nephrotic syndrome) and 24 healthy volunteers. We excluded patients with diabetes, cardiovascular disease and those with glomerulonephritis with an estimated GFR (eGFR) < 30 mL/min/1.73 m2. In addition to routine hematological and biochemical tests, plasma oxalate concentration, urinary oxalate excretion, and serum interleukin (IL)-6 and monocyte chemoattractant protein-1 (MCP-1) levels were assessed in all study participants.
Results. We observed that plasma oxalic acid concentration was significantly higher in patients with glomerulonephritis (19.0 [5.9–45.2] µmol/L) than in healthy volunteers (5.5 [3.8–7.3] µmol/L, p < 0.0001). Moreover, nephrotic proteinuria was significantly associated with plasma oxalic acid elevation independent of the patients’ age, sex, glomerular filtration rate, and body mass index (odds ratio = 1.42, 95% confidence interval = 1.13–1.77, p = 0.002). In turn, the increased plasma oxalic acid concentration was associated with high levels of serum IL-6 and MCP-1, which may be cardiovascular risk factors in patients with primary glomerulonephritis.
Conclusions. Nephrotic proteinuria was significantly associated with the elevation of plasma oxalic acid concentration and hyperoxaluria in glomerulonephritis patients with CKD stages 1–3b. Plasma oxalate at least partly promotes inflammation, which may be a cardiovascular risk factor in patients with glomerulonephritis in the early stages of CKD. Future studies should recruit at least 156 participants to confirm our preliminary results, validate nephrotic proteinuria as a risk factor for oxalate metabolism violation or determine the role of impaired oxalate homeostasis in clinical outcomes in patients with glomerulonephritis.
Objective. We hypothesized that an increase in the production of interleukins (IL)-6 and IL-17 could serve as a potential mechanism linking pre-existing uncontrolled blood pressure (BP) to the occurrence of long-COVID sequelae in patients undergoing hemodialysis (HD).
Methods. In this cross-sectional study, we examined serum IL-6 and IL-17 levels in 80 patients undergoing HD, taking into account preinfection BP, the presence of long-COVID sequelae, and the time interval after acute COVID-19 infection, which was either 5 or 10 months. The cytokines were measured by ELISA assay. Controlled BP was defined as a 3-month average pre-dialysis BP <140/90 mmHg and post-dialysis <130/80 mmHg.
Results. The prevalence of long-COVID sequelae was significantly higher in patients with uncontrolled BP than in the BP-controlled group. Both IL-6 and IL-17 concentrations were also significantly higher in patients with uncontrolled BP compared with the BP-controlled group. The patients with long-COVID sequelae had higher IL-6 and IL-17 values than the fully recovered patients at both time points, but their concentrations decreased significantly over time.
Conclusions. Elevated levels of serum IL-6 and IL-17 in patients undergoing HD with pre-existing uncontrolled BP may be associated with developing long-COVID sequelae.
233Intestinal colonization resistance is associated with hyperoxaluria in the patients with recurrent pyelonephritis
Eur Urol Suppl 2017; 16(3);e402Stepanova N.,
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