Citric acid monohydrate 334mg/5ml / Potassium citrate monohydrate 550mg/5ml / Sodium citrate dihydrate 500mg/5ml oral solution

PurposeTo evaluate the potential stone-preventative effects of apple cider vinegar (ACV) supplementation on 24-h urinary citrate, pH, and volume.MethodsWe performed a randomized crossover trial testing ACV, coconut water, lemon water, and orange soda. Participants were non-stone formers randomized to two of the four beverages. Participants consumed one assigned beverage daily for one week, underwent a two-week washout period, and then consumed the second assigned beverage. Three 24-h urine collections were planned: one baseline collection prior to beverage consumption, one following completion of the first treatment week, and one following completion of the second week.ResultsTwenty participants were enrolled. Eight were female. Six consumed ACV, six coconut water, eight lemon water, and six diet orange soda. ACV did not significantly change 24-h urinary parameters. Coconut water (+ 273.8 mg/24 h, 95% CI 67.9-480 mg/24 h) and lemon water (+ 167.7 mg/24 h, 95% CI 16-319 mg/24 h) were associated with increased urinary citrate. Effects on urine pH and volume were not significant in any treatment arms.ConclusionACV did not significantly change 24-h urine parameters. Coconut water and lemon water increased urinary citrate. Further study is necessary to validate these findings in a larger cohort. Registered with ClinicalTrials.gov (NCT04073719, 8/28/2019).

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Divalent cations such as calcium and ferrous sulfate interfere with the absorption of levothyroxine due to complexing. To our knowledge, the effects of magnesium on levothyroxine absorption have never been studied. The open-label cross-over pharmacokinetic study was conducted in 15 healthy, euthyroid adults. 1 mg of levothyroxine was administered in tablet form alone or co-administered with either magnesium aspartate or magnesium citrate. Participants received all three treatments, separated by a washout period, but were randomly allocated 1:1:1 to one of three treatment sequences. We measured thyroxine (T4) over a 6-h period after ingestion. The primary endpoint was the area under the curve (AUC) of thyroxine; secondary endpoints were Cmax and Tmax. Coadministration of magnesium aspartate significantly reduced thyroxine AUC by 12% (geometric mean ratio, GMR = 0.88, 95% CI 0.81-0.95, p = 0.002) and coadministration of magnesium citrate reduced thyroxine AUC non-significantly by 7% compared with levothyroxine alone (GMR = 0.93, 95% CI 0.86-1.01, p = 0.076). Cmax was significantly reduced by 7% and Tmax was significantly increased by 17% when magnesium aspartate was co-administered. The changes in Cmax and Tmax were smaller when magnesium citrate was co-administered. In conclusion, magnesium reduces the absorption of levothyroxine. However, we found smaller effects compared to those already described for other divalent cations, possibly due to the liquid formulation. Hypothyroid patients should nonetheless take levothyroxine separated from magnesium-containing formulations, especially if TSH levels are desired to be within a narrow range. If taken together, magnesium citrate may be a better option than magnesium aspartate.

Abstract licence: CC BY-NC

BackgroundDapagliflozin (DAPA) has shown major nephroprotective effects, improving kidney metabolism and oxigenation. Lipidomics and metabolomics are powerful tools for understanding such effects, providing a comprehensive look at how SGLT2 inhibitors might change the metabolic landscape beyond their primary glucose-lowering action. We investigated changes in plasma metabolomic/lipidomic profile and urinary excretion of metabolites that could occur independent of increased diuresis.MethodsA two-armed, parallel-design, randomized clinical trial was conducted in subjects with type 2 diabetes and hypertension who received treatment with DAPA 10 mg/day or hydrochlorothiazide 12.5 mg/day for four weeks. Lipidomics and metabolomics were performed by high resolution mass spectrometry in fasting plasma and 24-hour urine samples collected before and after treatment.ResultsCompared to hydrochlorothiazide, DAPA significantly increased plasma isoleucine, methionine, citrate, β-hydroxybutyrate and decreased lactate. DAPA induced plasma lipid remodeling towards a significant raise in free fatty acids (FFAs) and some sphingomyelins and lysophosphatidylcholines containing these fatty acids. A significant change was observed in plasma medium- and short-chain acylcarnitines, positively correlated with changes in plasma FFAs and β-hydroxybutyrate. In addition, DAPA, but not hydrochlorothiazide, significantly increased 24-h urinary excretion of several amino-acids, lactate, TCA cycle metabolites, β-hydroxybutyrate and electrolytes, except for a decrease in malate excretion.ConclusionsDAPA treatment has major effects on the plasma lipidomic and the urine metabolomic profiles, with significant increased renal excretion of several metabolites, especially amino-acids, independently of increased diuresis. These data offer insights into the complex metabolic pathways leading to kidney protection by SGLT2 inhibitors.Clinical trial informationEuropean Union Drug Regulating Authorities Clinical Trials No. 2015-004164-11.

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ObjectiveRegional citrate anticoagulation (RCA) is recommended as the first choice of anticoagulation strategies in continuous renal replacement therapy (CRRT). However, when using calcium-containing replacement fluid, whether RCA can achieve sufficient anticoagulant effect among different CRRT modalities remains unclear.Materials and methodsIn this open-label, three-arm, randomized trial, AKI patients receiving RCA-CRRT with calcium-containing replacement fluids were randomized to continuous veno-venous hemofiltration (CVVH), continuous veno-venous hemodialysis (CVVHD) and continuous veno-venous hemodiafiltration (CVVHDF) groups from 2022 to 2023. The primary outcomes were circuit lifespan and early circuit failure. Secondary endpoints included the safety of the three groups and 30-day all-cause mortality.ResultsA total of 121 patients were enrolled, with 40 in CVVH group, 40 in CVVHD group, and 41 in CVVHDF group. The circuit lifespan in CVVHDF group (70 h, IQR 65-72) was significantly longer than that in CVVHD (47 h, IQR 31.5-54) and CVVH group (64 h, IQR 46-71) (P ConclusionOur findings suggested that RCA-CRRT with calcium-containing replacement solution appeared to be safe and effective, with CVVHDF showing potentially prolonged filter survival compared to alternative modalities, which might support its consideration as a possible option in clinical practice.Trial registrationThis study was registered in the Chinese Clinical Trial Registry ( www.chictr.org.cn ) under the registration number ChiCTR2200061065 on 15 June 2022.

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BackgroundMedial arterial calcification (MAC) and increased arterial stiffness contribute to cardiovascular disease risk in type 2 diabetes mellitus (T2DM). Experimental studies suggest that magnesium supplementation may halt arterial calcification and improve arterial stiffness.ObjectivesThis study aimed to evaluate the effect of 6-mo oral magnesium citrate supplementation on calciprotein crystallization (T50) and carotid-femoral pulse wave velocity (cfPWV) in individuals with T2DM and peripheral MAC.MethodsThis double-blind, placebo-controlled trial randomly assigned 74 participants with T2DM [78% males, 72 (68-76) y] with peripheral MAC and cfPWV≥12.0 m/s to magnesium citrate (350 mg/d; n = 37) or placebo (n = 37). Nephelometry-based T50 measurements, cfPWV measurements, and 24-h urine collections were obtained at baseline, 3 and 6 mo. Longitudinal analysis of covariance adjusted for baseline T50 and cfPWV was used to study the treatment effects on T50 and cfPWV.ResultsBaseline mean T50 and cfPWV were similar between the magnesium group (T50 348 ± 54 min; cfPWV 15.9 ± 2.2 m/s) and the placebo group (362 ± 54 min; 15.6 ± 2.0 m/s). Magnesium in serum and in 24-h urine were lower in the magnesium group [0.74 (0.71-0.77) mmol/L and 3.30 (2.06-4.71) mmol/24 h] compared with the placebo group [0.81 (0.74-0.86) mmol/L and 4.31 (3.09-5.54) mmol/24 h]. Supplementation increased 24-h urine magnesium excretion (P 50 [ẞ = 6 min (-11, 22), P = 0.491] but did increase cfPWV [ẞ = 0.8 m/s (0.1, 1.5), P = 0.021] over 6 mo in the magnesium group relatively to the placebo group, but the statistical significance was lost after adjusting for clinically relevant baseline differences [T50: ẞ = 7 min (-12, 25), P = 0.482; cfPWV: ẞ = 0.5 m/s (-0.2, 1.3), P = 0.180].ConclusionsSix-month magnesium citrate supplementation did not reduce calciprotein crystallization and arterial stiffness in older individuals with T2DM with peripheral MAC. Daily supplementation of 350 mg appears to be ineffective in this population, possibly attributable to normomagnesemia and preserved renal function. This study was registered at the Dutch Trial Register (CCMO) as NL81281.029.22 and at ISRCTN as 60460377.

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