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.

The present study aimed to evaluate the changes in oxidative stress markers according to the concentration of plasma oxalic acid (POx) in end-stage renal disease (ESRD) patients. Methods. We conducted a cross-sectional observational study involving 72 ESRD patients and 30 relatively healthy individuals who served as a control reference group for evaluation of POx concentration. Among ESRD patients there were 32 hemodialysis (HD) patients and 40 peritoneal dialysis (PD). POx concentration was measured spectrophotometrically using a commercially available kit (MAK315, Sigma, Spain). Malonic dialdehyde (MDA), ceruloplasmin (CP), transferrin (TR), sulfhydryl groups (SH-groups), antioxidant blood capacity (AOC) and total peroxidase activity of erythrocytes (TPA) were measured and the oxidative stress index (OSI) was calculated in all examined patients. Results. A significant increase in POx concentration was observed in ESRD patients compared with healthy volunteers (p < 0.0001). The concentrations of MDA in serum, OSI in erythrocytes and serum of the examined patients were gradually increased, while serum levels of CP, AOC, SH-groups and TPA in erythrocytes, on the contrary, were decreased in accordance with the increasing trend of POx concentrations. Correlation analysis demonstrated a statistically significant direct relationship between POx concentration and MDA (r = 0.57; p <0.0001) and OSI (r = 0.64; p <0.0001). The inverse correlation was determined between POx and antioxidant markers: CP (r = -0.35; p = 0.007), SH-groups in serum (r = -0.3; p = 0.04) and erythrocytes (r = -0.53 ; p <0.0001). Conclusions. The intensity of oxidative-antioxidant balance disorders in the blood of ESRD patients has been associated with the POx concentration: the higher the concentration of POx was the more active oxidative processes and the more pronounced lack of antioxidant protective factors occurred. Further studies are needed to determine the role of POx in the initiation of oxidative stress and chronic inflammation in ESRD patients.

Introduction. The effect of serum uric acid (SUA) concentration on residual urine volume in peritoneal dialysis (PD) patients has not been postulated yet. The present study aimed to investigate the effect of SUA concentration on residual diuresis in PD patients. Methods. It was a retrospective observational study involving 175 patients who were treated with PD for at least 3 months. The primary study outcome was residual dieresis decline<100 mL/24h represented as the time to onset of anuria. Results. A total of 175 PD patients with the median PD vintage of 13.5 [5.0-19.7] months before the enrollment were included in the study. Among the participants, there were 79 (45.2%) men and 96 (54.8%) women. Hyperuricemia was found in 48/79 (60.8%) men and 39/96 (40.6%) women (p=0.008). Residual renal function was significantly lower in the PD patients with hyperuricemia compared with the hyperuricemia-free patients. During a 22.5 [15.8-28.3] month follow-up period, 64 (42.3%) PD patients progressed to anuria and its prevalence was significantly higher in the hyperuricemic group compared with the normouricemic group (64.3% vs 20.4%, p <0.001). The multivariate logistic regression analysis demonstrated that hyperuricemia was an independent risk factor associated with the development of anuria in PD patients. The additional Cox regression analysis confirmed hyperuricemia as a predictor for anuria development in the PD patients: HR 2.6 (95% CI 1.38; 4.9), p=0.003. Conclusions. Hyperuricemia is an independent risk factor for residual diuresis decline < 100 mL/24h in PD patients.

Background: Little evidence is available on oxalate balance in peritoneal dialysis (PD) patients. Patients and Methods: We performed a cross-sectional observational pilot study with 62 adult PD patients to document oxalate balance and explore its association with PD-related peritonitis. Plasma oxalate concentration, levels of oxalate excretion in 24-h urine, and peritoneal dialysis effluent were evaluated. The peritoneal oxalate transport status and renal and peritoneal oxalate clearances were calculated according to the PD-related peritonitis history. Results: PD patients with a history of peritonitis had a statistically significantly lower peritoneal oxalate clearance, daily peritoneal oxalate excretion, and overall oxalate removal rate compared with the peritonitis-free PD patients. They had a 4-fold risk of plasma oxalic acid increase, and even a single episode of dialysis-related peritonitis resulted in plasma oxalate elevation. Conclusion: Peritoneal oxalate clearance plays an important role in oxalate balance in PD patients and, therefore, dialysis-related peritonitis is a significant predictor for hyperoxalemia. Further well-designed clinical trials need to be undertaken before the association between peritonitis and oxalate balance in PD patients is more clearly understood.Oxalate is an ionized form of a potentially toxic oxalic acid formed from endogenously synthesized and exogenously ingested oxalates (1, 2). In physiological conditions, the bulk of circulating oxalate (90-95%) is excreted through the kidneys, whereas the remainder (5-10%) through the terminal parts of the small intestine and colon (1-4). A decline in kidney function leads to decreased oxalate clearance and, ultimately, hyperoxalemia in end-stage kidney disease (ESKD) (1, 5-7). The accumulation of oxalate is associated with oxidative stress and systemic inflammation (1, 8, 9), high cardiovascular risk (9-11), and increased mortality rate (1, 11) in patients with kidney stones and ESKD. Nevertheless, little evidence is available on oxalate balance in ESKD patients in general and peritoneal dialysis (PD) patients in particular; almost all scientific data on this issue were published during the 1980s and 1990s (6,(12)(13)(14).Worldwide, PD is a key element of kidney replacement therapy (15-17). Nonetheless, peritonitis remains one of the major challenges associated with severe clinical complications of PD despite technological advances (17,18). Detrimental effects of dialysis-related peritonitis on the characteristics of peritoneal transport and the alterations of the peritoneal membrane have been documented (19-21). However, the potential effect of dialysis-related peritonitis on oxalate balance in PD patients has never been evaluated before. We hypothesized that the alteration of the peritoneal membrane due to dialysis-related peritonitis could decrease the peritoneal clearance of oxalate and, consequently, its removal levels. To test this hypothesis, the present study aimed to define oxalate balance and explore its association with dia...

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.