Sodium bicarbonate 2.623g / Sodium citrate 939mg effervescent granules sachets

INTRODUCTION: Chronic kidney failure (CKD), a common cause of mortality, impacts about 800 million individuals globally. Metabolic acidosis, which occurs in 20% of people with CKD, complicates the course of CKD and increases the possibility of morbidity and mortality in these patients. Veverimer, a promising experimental acid-binding polymer that may be taken orally and has a high capacity, presents a unique method for the management of metabolic acidosis conditions in CKD patients. This study aimed to assess the safety and effectiveness of veverimer compared to placebo by analysing data from randomised controlled trials. METHODS: A systematic review and meta-analysis were conducted following PRISMA guidelines. Databases searched included PubMed, Scopus, Web of Science, Embase, clinicaltrials.gov, and Cochrane CENTRAL until April 24th, 2025. Our analysis comprised randomised controlled trials that assessed the impact of veverimer on patients with CKD and metabolic acidosis. Quality assessment was performed using the Joanna Briggs Institute (JBI) assessment. RESULTS: Four studies met the inclusion criteria. A total of 1083 participants were randomly assigned to receive veverimer, whereas 945 participants were given a placebo. Veverimer was able to significantly increase serum bicarbonate compared to the placebo group (mean difference = 2.90 mmol/L (95% CI: 2.15 to 3.65, p < 0.01)). The adverse events in the veverimer group did not differ significantly from the placebo group. Meta-regression showed that mean age and mean GFR did not have a statistically significant association with the treatment effect. DISCUSSION AND CONCLUSION: In conclusion, our study offers robust support for the use of veverimer in treating metabolic acidosis, while also identifying areas that require additional investigation. The results of this study may inform future research and clinical practices in managing metabolic acidosis. CLINICAL TRIAL: N/A.

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Background: Metabolic acidosis (MA) is frequently associated with chronic kidney disease (CKD) progression. Our aim was to compare the effect of oral sodium citrate (SC) with that of oral sodium bicarbonate (SB) on renal function and serum bicarbonate correction, as well as to evaluate their safety profile in patients with MA of CKD. Methods: We conducted a prospective, single-center, randomized 1:1, parallel, controlled, unblinded clinical trial of 124 patients with MA and CKD stages 3b and 4. The primary outcome was the mean change in estimated glomerular filtration rate (eGFR). The secondary outcomes were mean change in serum bicarbonate level, eGFR decrease by 30%, eGFR decrease by 50%, dialysis, death or prolonged hospitalization, and a combined endpoint. Results: No significant difference was found between the groups in terms of mean eGFR change [adjusted mean difference = −0.99 mL/min/1.73 m2 (95% CI: −2.51 to 0.93, P = .20)]. We observed a mean serum bicarbonate change of 6.15 mmol/L [(95% CI: 5.55–6.74), P < .001] in the SC group and of 6.19 mmol/L [(95% CI: 5.54–6.83), P < .001] in the SB group, but no significant difference between the 2 groups [adjusted mean difference = 0.31 mmol/L (−0.22 to 0.85), P = .25]. Cox proportional hazard analysis showed similar risks regarding eGFR decrease by 30% (P = .77), eGFR decrease by 50% (P = .50), dialysis (P = .85), death or prolonged hospitalization (P = .29), and combined endpoint (P = .57). Study drug discontinuation due to adverse events was significantly more common in the SB group (17.7% vs 4.8%, P = .02). Conclusions: SC and SB have a similar effect on kidney function decline, both improve serum bicarbonate level, but SB is associated with higher rates of medication discontinuation due to adverse events.

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IntroductionMetabolic acidosis may create a pathway to cognitive impairment in chronic kidney disease (CKD) by contributing to cerebrovascular dysfunction. Trials examining the effect of sodium bicarbonate (NaHCO3) on cognitive function are lacking.MethodsWe conducted a randomized, double-blind, placebo-controlled pilot study examining the effect of 12 months of NaHCO3 on cognitive function in 34 patients aged 50-80 years with CKD stage 3b-4 (eGFR 15-44 ml/min/1.73m2) with metabolic acidosis (serum bicarbonate level 16-22 mEq/L). Participants were randomized 1:1 to NaHCO3 or placebo. The primary endpoint was change in overall cognition (Cognitive Function Composite score) assessed by the NIH Toolbox® Cognition Battery over 12 months. Secondary endpoints were change in cerebrovascular reactivity and pulsatility of the middle cerebral artery (MCA) assessed by Transcranial Doppler Ultrasonography over 12 months.Results33 patients completed the study. After 12 months of treatment with NaHCO3 therapy, the Cognitive Function Composite score increased significantly from baseline (mean ± SD, 47.3 ± 8.5 to 49.3 ± 11.0, p = 0.03), however, there was no difference compared to placebo (p = 0.39). NaHCO3 therapy resulted in a significant reduction in time to perform the Trail Making Test-A (median [IQR], 31.3 [27.0, 36.3] to 29.0 [19.4, 38.2] seconds, p = 0.02), however there was no difference compared to placebo (p = 0.29). After 12 months of treatment, there was a significant increase in resting pulsatility index of the MCA in the placebo group, but there were no statistical differences between groups (p = 0.71). NaHCO3 treatment resulted in a significant decrease in baseline mean blood flow velocity of the MCA (p = 0.03), but there was no difference from placebo (p = 0.11).ConclusionsAlthough there were trends supporting a role for sodium bicarbonate in having an effect on cognitive function, this was not significant in this underpowered study. A larger study is recommended.Trial registrationClinicaltrials.gov (NCT04600323) on 10/19/2020.

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IntroductionFor critically ill patients requiring continuous renal replacement therapy, regional citrate anticoagulation is the preferred strategy to maintain extracorporeal circuit patency. Current clinical practice relies on two citrate-based protocols, with the widely used but complex 4% trisodium citrate solution posing a hypernatraemia risk and haemofiltration replacement fluid of sodium citrate offering procedural simplification and a more physiological electrolyte profile. Direct prospective comparison of their circuit lifespan efficacy is currently unavailable.Methods and analysisThis single-centre, prospective, open-label, parallel-group randomised controlled trial will be conducted in China. 90 patients will be enrolled and randomly assigned (1:1) to receive anticoagulation with either citrate-based haemofiltration replacement fluid or 4% trisodium citrate solution, with all patients undergoing a standardised continuous venovenous haemofiltration protocol. The primary outcome is circuit lifespan, with a non-inferiority margin set at 2.43 hours. Secondary outcomes include the 72-hour circuit survival probability, duration of hospitalisation, and all-cause mortality rates at 28 and 90 days. The primary analysis will follow the intention-to-treat principle.Ethics and disseminationThe study protocol has been approved by the Biomedical Research Ethics Committee of West China Hospital, Sichuan University (Approval No. (2025)1157). Any subsequent amendments must be submitted to the same ethics committee for further review and approval prior to implementation. Furthermore, the findings of this trial will be disseminated through presentations at relevant national and international conferences and via publication in peer-reviewed scientific journals.Trial registration numberChinese Clinical Trial Registry ChiCTR2500106991.

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