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.
<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.
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...
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 influence 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 oxalate-degrading 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 oxalate-degrading 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 significantly 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 beneficial effect on the total oxalate-degrading activity of gut microbiota, which resulted in decreased UOx excretion in rats.
Patients undergoing hemodialysis (HD) are at increased risk of severe complications from COVID-19 due to compromised immune function and comorbidities. This retrospective study aimed to investigate the association between pre-existing serum indoxyl sulfate (IS) concentrations and COVID-19 outcomes in HD patients. Methods. Data on pre-existing IS and proinflammatory cytokines, such as interleukin-6 (IL-6), monocyte chemoattractant protein-1 (MCP-1), and tumor necrosis factor-alpha (TNF-α) were extracted from an existing patient database. The patients were followed up for 1.5 years and compared according to median serum IS concentration: low-IS (< 22.2 μg/mL) and high-IS (≥22.2 μg/mL) groups. The primary outcomes focused on assessing the risk and severity of COVID-19 infection. Results. A total of 56 patients aged 62 (56-67) years with a dialysis vintage of 37.5 (30-168) months were included in the analysis. Serum levels of IS were significantly correlated with Kt/V values (p = 0.043), arterial hypertension (p = 0.001), IL-6 (p = 0.023), MCP-1 (p = 0.023), and TNF-α (p = 0.033) concentrations. Elevated serum IS levels were significantly associated with an increased risk of COVID-19 infection (p < 0.0001) and a higher likelihood of hospitalization (p = 0.03). Patients with higher IS levels exhibited more severe lung involvement (p < 0.0001) and a greater need for respiratory support (p = 0.004). A serum IS concentration of 21.5 μg/mL was the optimal threshold for predicting COVID-19 infection in HD patients (sensitivity of 83.4% and specificity of 92.3%, p < 0.0001). Conclusion: Our study highlights the detrimental impact of serum IS on COVID-19 infection and its clinical outcomes in patients undergoing HD. Further research is warranted to elucidate the underlying mechanisms and explore potential therapeutic strategies targeting IS in this population.
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