Potassium citrate 282mg / Potassium bicarbonate 527mg modified-release granules sachets sugar free

BackgroundRecurrent urolithiasis is a major clinical challenge, with more than 50% of patients experiencing recurrence within 5 years. While potassium citrate effectively reduces recurrence, poor adherence due to cost and gastrointestinal side effects limits its long-term use. Citrus-based interventions, such as lime juice, have shown potential in enhancing urinary citrate and alkalinity but require further validation. This study evaluated the efficacy of a lime-based phytochemical-rich regimen (LPR) in preventing stone recurrence and reducing urinary inflammation in post-operative urolithiasis patients.ObjectiveThis multicenter, double-blind, randomized controlled trial aimed to evaluate the efficacy and safety of a novel lime-based preparation called LPR in preventing kidney stone recurrence over 24 months.MethodsIn a double-blind, randomized, placebo-controlled, multicenter trial, 173 patients with calcium oxalate urolithiasis who had undergone successful stone removal were enrolled from six hospitals in Thailand. Participants were randomized to receive either LPR or placebo for 24 months. The primary outcome was the incidence of stone recurrence confirmed by computerized topography (CT). Secondary outcomes included changes in urinary protein excretion and urinary interleukin-8 (IL-8) level, a pro-inflammatory cytokine implicated in renal inflammation and stone formation. Kaplan-Meier survival analysis and multivariate Cox regression were used to assess recurrence risk.ResultsOf 173 enrolled participants, 151 completed the study. The recurrence rate at 2 years was significantly lower in the LPR group (14%) compared to placebo (45%) (p ConclusionLPR, a lime-based supplement rich in citrate and flavonoids, significantly reduced the 2-year recurrence rate of calcium oxalate stones by approximately 76%. This effect may be mediated by increased urinary citrate excretion, alkalinization, and attenuation of renal inflammation, as evidenced by reduced urinary IL-8 and proteinuria. LPR was well tolerated, with minimal adverse effects, and may serve as a safe, cost-effective adjunct for secondary prevention in patients intolerant to conventional alkali therapy.

Abstract licence: CC BY

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.

Abstract licence: CC BY-NC-ND