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Journal of Pharmaceutical Health Care... May 2024Fruits and vegetables are abundant in alkali precursors and effectively reduce the Potential Renal Acid Load (PRAL) from diet. Oral alkali supplements are supposed to...
BACKGROUND
Fruits and vegetables are abundant in alkali precursors and effectively reduce the Potential Renal Acid Load (PRAL) from diet. Oral alkali supplements are supposed to exert comparable alkalizing effects on the human body, and have been shown to beneficially affect bone and kidney health. A comparative analysis of the available dietary alkali supplements in Germany was performed, contrasting their potential PRAL-lowering potential.
METHODS
We reviewed the currently available dietary citrate-based alkali supplements sold in Germany with a special focus on their mineral content, their PRAL-lowering potential and other characteristics inherent to each product. Supplements containing either potassium-, calcium- or magnesium citrate or any combination of these organic salts were reviewed. The total alkali load (TAL) was calculated based on the recommended daily dosage (RDD).
RESULTS
Sixteen supplements with a mean alkali powder content of 220.69 ± 111.02 g were identified. The mean magnesium content per RDD was 239.93 ± 109.16 mg. The mean potassium and median calcium content were 550 ± 325.58 mg and 280 (240) mg, respectively. Median TAL was 1220 (328.75) mg. The PRAL-lowering potential from a single RDD ranged from - 51.65 mEq to -8.32 mEq. Substantial price differences were found, and the mean price of the examined supplements was 16.67 ± 5.77 Euros. The median price for a 1 mEq PRAL-reduction was 3.01 (3.14) cents, and ranged from 0.77 cents to 10.82 cents.
CONCLUSIONS
Noticeable differences between the identified alkali supplements were encountered, warranting an individual and context-specific approach in daily clinical practice.
PubMed: 38730472
DOI: 10.1186/s40780-024-00342-0 -
Archivos Espanoles de Urologia Oct 2021In this article already published, it has been detected that in the summary, on page 112 where it says "water" itshould say "fluid". The corrected text is as...
In this article already published, it has been detected that in the summary, on page 112 where it says "water" itshould say "fluid". The corrected text is as follows:Nutrition is tightly associated with the risk of stone events. Apart from genetic predisposition, a correct and balanced diet might prevent incident kidney stones. Several studies analyzed each dietary component and different diets to better understand their impact on stone recurrence. Fluids: High fluids intake is the most important factor for preventing kidney stones disease and for every 200 mL of fluid, the risk of stones is reduced by 13%. Soft drinks seems to be associated to a greater risk of stone events, whereas caffeine and citrus fruits juice are not.Calcium: Normally calcium intake with diet does not exceed 1.2 g/day. A balanced consumption of dairy products is capable of reducing oxalate intestinal absorption and urinary excretion compared to low calcium diet, being protective for stone disease. Oxalate: The exact amount of oxalate contained in different foods is difficult to estimate for its variability, even in the same aliment. In addition, the amount of oxalate consumed was shown to be only a minor risk factor for stone disease, whereas its intestinal absorption is strongly influenced by external factors, such as calcium intake. Dietary oxalate restriction is advisable only in patients with known elevated consumption. Sodium: High sodium intake is both associated with hypertension, heart disease and stone risk. Increased sodium consumption is directly associated to hypercalciuria in both calcium stone formers and healthy subjects. Although dietary sodium restriction to recommended values is always desirable in stone formers, it is difficult to achieve for its broad use in food preparation. Proteins: Animal proteins are associated to increased risk for stone formation, whereas vegetable and dairy proteins are not. Increased meat intake was associated to acidic urine pH, negative calcium balance and reduced anti-lithogenic urinary solutes excretion. Fruits and vegetables: Alkalizing foods are one of the most important factors for stone protection. Their consumption increases anti-lithogenic solutes as citrate, potassium and magnesium. A diet rich in fruits and vegetables is strongly recommended for stone formers. Uric acid: Elevated meat consumption is either associated to increased purine metabolism and acid load, favoring uric acid nephrolithiasis by reducing urine pH and increasing urinary excretion of uric acid, especially in patients affected by metabolic syndrome and diabetes.In conclusion, the most effective diet for stone protection is rich in fruits and vegetables, low in animal proteins and salt, with balanced dairy product consumption and obviously, with elevated fluid intake. These characteristics make vegetarian and Mediterranean diets protective and useful for stone formers, whereas western diet is at risk for stone formation.
Topics: Calcium; Calcium, Dietary; Dietetics; Humans; Kidney Calculi; Life Style; Sodium, Dietary
PubMed: 34605410
DOI: No ID Found -
BMC Nephrology Apr 2020Aciduria caused by urinary excretion of acidic metabolic wastes produced in daily life is known to be augmented in patients with chronic kidney disease (CKD). To...
BACKGROUND
Aciduria caused by urinary excretion of acidic metabolic wastes produced in daily life is known to be augmented in patients with chronic kidney disease (CKD). To evaluate the reno-protective effect of oral alkalizing agents for the improvement of metabolic acidosis and neutralization of intratubular pH in the patients with mild stages of CKD. Also, to identify reno-protective surrogate markers in the serum and urine that can closely associate the effect of urine alkalization.
METHODS
In this single-centered, open-labeled, randomized cohort study, patients with CKD stages G2, G3a and G3b, who visited and were treated at Tohoku University Hospital during the enrollment period were registered. We administered sodium bicarbonate or sodium-potassium citrate as the oral alkalinizing agents. A total of 150 patients with CKD will be randomly allocated into the following three groups: sodium bicarbonate, sodium-potassium citrate and standard therapy group without any alkalinizing agents. The data of performance status, venous blood test, spot urine test, venous blood-gas test, electrocardiogram, renal arterial ultrasonography and chest X-ray will be collected at 0, 6, 12 and 24 weeks (short-term study) from starting the interventions. These data will be also collected at 1 and 2 years (long-term study). The samples of plasma and serum and early-morning urine at every visit will be acquired for the analysis of renal function and surrogate uremic biomarkers. The recruitment for this cohort study terminated in March, 2018, and the follow-up period for all the enrolled subjects will be terminated in December, 2020. The primary endpoint will be the development of originally-defined significant renal dysfunction or the occurrence of any cerebrovascular disease in the short-term study. The secondary endpoint will be the same endpoints as in the long-term study, or the patients with significant changes in the suggested the surrogate biomarkers.
DISCUSSION
The findings of this study will address the importance of taking oral alkalizing agents in the patients with early stages of CKD, furthermore they could address any new surrogate biomarkers that can be useful from early stage CKD.
TRIAL REGISTRATION
Registered Report Identifier: UMIN000010059 and jRCT021180043. The trial registration number; 150. Date of registration; 2013/02/26.
Topics: Acidosis; Administration, Oral; Adult; Antacids; Biomarkers; Drug Monitoring; Female; Humans; Male; Potassium Citrate; Protective Agents; Randomized Controlled Trials as Topic; Renal Elimination; Renal Insufficiency, Chronic; Sodium Bicarbonate; Sodium Citrate
PubMed: 32321450
DOI: 10.1186/s12882-020-01807-8 -
Biological & Pharmaceutical Bulletin 2021Extracellular pH (pHe) of tumor cells is characteristic of tumor microenvironment (TME). Acidic TME impairs the responses of tumors to some anti-cancer chemotherapies....
Neutralization of Acidic Tumor Microenvironment (TME) with Daily Oral Dosing of Sodium Potassium Citrate (K/Na Citrate) Increases Therapeutic Effect of Anti-cancer Agent in Pancreatic Cancer Xenograft Mice Model.
Extracellular pH (pHe) of tumor cells is characteristic of tumor microenvironment (TME). Acidic TME impairs the responses of tumors to some anti-cancer chemotherapies. In this study, we showed that daily oral dosing of sodium potassium citrate (K/Na citrate) increased blood HCO concentrations, corresponding to increase of HCO concentrations and pHs in urine, and neutralized the tumor pHe. Neutralization of acidic TME by alkaline substance like HCO, an active metabolite of K/Na citrate, well potentiated the therapeutic effect of anticancer agent TS-1, an orally active 5-fuluoro-uracil derivative, in Panc-1 pancreatic cancer-xenograft murine model. Neutralization of acidic TME by using an alkaline K/Na citrate is a smart approach for enhancement of the therapeutic effects of anticancer agents for pancreatic cancer in the end stage.
Topics: Administration, Oral; Animals; Antacids; Cell Line, Tumor; Drug Combinations; Drug Synergism; Extracellular Space; Female; Humans; Hydrogen-Ion Concentration; Mice; Oxonic Acid; Pancreatic Neoplasms; Potassium Citrate; Sodium Citrate; Tegafur; Tumor Microenvironment; Xenograft Model Antitumor Assays
PubMed: 33518679
DOI: 10.1248/bpb.b20-00825 -
American Journal of Translational... 2023Potassium voltage-gated channel subfamily Q member 1 (KCNQ1), is implicated in the onset and progression of gastric carcinoma (GC), one of the most common types of...
BACKGROUND
Potassium voltage-gated channel subfamily Q member 1 (KCNQ1), is implicated in the onset and progression of gastric carcinoma (GC), one of the most common types of stomach malignancies. This research aims to investigate the potential prognostic implications of KCNQ1 mRNA in GC using various databases such as The Cancer Genome Atlas (TCGA), The Human Protein Atlas (HPA), LinkedOmics, TISIDB, ESTIMATE, and TIMER.
METHODS
We searched the HPA database to obtain information on KCNQ1 levels in human normal tissues, organs, and cell lines as well as in pan-cancer tissues. Then, we used TIMER and UALCAN to comparatively analyze the KCNQ1 mRNA levels in different types of cancers relative to their adjacent normal counterparts. Based on TCGA and Gene Expression Omnibus, the correlation of clinical information with KCNQ1 expression was analyzed using logistic regression model. Univariable and Multivariate Cox analyses were then carried out to compare differences in survival among patients with different clinical characteristics. The multivariate methods, such as Kaplan-Meier plotter and GEPIA survival curves, were further employed to identify the correlation of KCNQ1 expression with overall survival (OS). Besides, LinkedOmics was used to identify differentially expressed genes for functional enrichment analysis.
RESULTS
KCNQ1 exhibited tissue-specific imprinting and expression in human normal tissues, organs and cell lines, while it was aberrantly expressed in pan-cancer tissues. Lower KCNQ1 mRNA expression was determined in GC tissue samples versus normal counterparts. In GC cases, elevated KCNQ1 levels were strongly linked to a longer OS and strongly correlated with invasion depth (χ=12.631, P=0.006), TNM stage (χ=8.750, P=0.033), differentiation grade (χ=7.426, P=0.024), and vital status (χ=5.676, P=0.017). Furthermore, KCNQ1 was identified by univariable and multivariate Cox analyses as an independent risk factor for GC. Based on Gene Ontology analysis, digestion as well as tricarboxylic acid metabolic, carbohydrate catabolic, and small molecule catabolic processes were differentially enriched in the up-regulated KCNQ1 phenotypic pathway. While carbon metabolism, fatty acid degradation, peroxisome, and citrate cycle (TCA cycle) were identified by the Kyoto Encyclopedia of Genes and Genomes-based analysis as pathways with differential enrichment.
CONCLUSION
Being a prognostic biomarker, KCNQ1 may play an inhibitory role and involve in the metabolic process of GC.
PubMed: 37434821
DOI: No ID Found -
Journal of Dairy Science Jan 2021Calf diarrhea can commonly lead to dehydration and metabolic acidosis due to the loss of fluid and electrolytes. The objective of this randomized clinical trial was to...
Calf diarrhea can commonly lead to dehydration and metabolic acidosis due to the loss of fluid and electrolytes. The objective of this randomized clinical trial was to examine differences between treating male dairy calves experiencing diarrhea with either a basic bicarbonate electrolyte powder (BBP) composed of sodium bicarbonate (50.7 mmol/L); a mixed buffer powder (MBP) including sodium bicarbonate (33.8 mmol/L), sodium citrate (8.4 mmol/L), sodium acetate (6.3 mmol/L), and potassium citrate (1.9 mmol/L); or a liquid electrolyte (HAL) composed of sodium acetate (50.1 mmol/L). All 3 electrolyte solutions were standardized to provide 50 mmol/L blood buffers and a similarly strong ion difference (74.4, 74.9, and 82.6 mEq/L for BBP, MBP, and HAL, respectively). Holstein male calves (n = 80) were sourced from auction barns or local farms and delivered in 1 batch to the research facility. Calves were housed in individual pens and fed a 24% crude protein and 17% fat calf milk replacer (CMR) twice daily. Starter grain and water were offered ad libitum. Calves were randomly enrolled in 1 of the 3 treatments when experiencing either 2 consecutive days of a fecal score of 2 (runny, spreads easily) or 1 d with a fecal score of 3 (liquid devoid of solid material). Calves were blocked by the different enrollment criteria. The respective electrolyte solution was administered via esophageal tube 1 h after feeding CMR until the fecal score returned to 0 (normal consistency) or 1 (semiformed or pasty). Blood gas measurements were taken at 1, 8, and 24 h post the initial electrolyte feeding, and weight was measured at 1, 2, 7, 14, and 28 d postenrollment. Mixed repeated measure linear regression models were built to assess the effect that the electrolyte solutions had on the blood gas measurements and body weight. A total of 45 calves were enrolled in the trial with 14, 16, and 15 calves randomly assigned to the MBP, HAL, and BBP groups, respectively. As compared with BBP, MBP increased blood CO at 8 and 24 h, increased bicarbonate at 24 h, increased base excess at 8 and 24 h, and increased anion gap at 24 h. Calves in the BBP and HAL groups noted more severe eye recession when compared with the MBP group. Average daily gain did not differ between treatments at any time point. Although a severe dehydration challenge was not present, which should be considered a limitation of the study, MBP improved the acid-base status of calves compared with BBP, whereas HAL performed similarly to MBP.
Topics: Animal Feed; Animals; Body Weight; Cattle; Cattle Diseases; Diarrhea; Diet; Electrolytes; Feces; Male; Milk; Sodium Acetate; Sodium Bicarbonate
PubMed: 33189262
DOI: 10.3168/jds.2020-18526 -
CEN Case Reports Aug 2022A 7-month-old male infant was referred to us for evaluation of hypercalcemia and failure to thrive. He was the second-born child to third-degree consanguineous parents...
A 7-month-old male infant was referred to us for evaluation of hypercalcemia and failure to thrive. He was the second-born child to third-degree consanguineous parents with a birth weight of 3.5 kg. The index child was severely underweight. Initial laboratory investigations showed hypercalcemia (13.6 mg/dL), hypophosphatemia, hyponatremia, hypokalemia and hypochloremia. The initial serum bicarbonate level was 20.9 mEq/L. The urine calcium: creatinine ratio (0.05) was normal. He was noted to have polyuria (6 mL/kg/hr) and required intravenous fluids to maintain intravascular volume and manage hypercalcemia, along with potassium chloride supplements. The serum calcium decreased to 9.7 mg/dL after hydration for 48 h. At this juncture, the child was noted to exhibit metabolic acidosis (serum bicarbonate 16 mEq/L) for the first time. Thereafter, fractional excretion of bicarbonate was estimated to be 16.5% while the tubular threshold maximum for phosphorus per glomerular filtration rate was 1.2 mg/dL; indicating bicarbonaturia and phosphaturia, respectively. Glycosuria with aminoaciduria were also noted. Clinical exome sequencing revealed a NM_004937.3:c.809_811del in exon 10 of the CTNS gene that resulted in in-frame deletion of amino acids [NP_004928.2:p.Ser270del] at the protein level. The child is now growing well on oral potassium citrate, neutral phosphate and sodium bicarbonate supplements. This case was notable for absence of metabolic acidosis at admission. Instead, severe hypercalcemia was a striking presenting manifestation, that has not been reported previously in literature. Cystinosis has been earlier described in association with metabolic acidosis, hypocalcemia and hypomagnesemia. However, typical features like metabolic acidosis were masked in early stages of the disease in our case posing a diagnostic challenge. This atypical initial presentation adds to the constellation of clinical features in this condition.
Topics: Acidosis; Bicarbonates; Calcium; Cystinosis; Humans; Hypercalcemia; Infant; Kidney Diseases; Male
PubMed: 35048353
DOI: 10.1007/s13730-021-00675-x -
International Journal of Molecular... Jan 2023The use of degrading enzymes in polymer formulation is a very attractive strategy to manage the end-of-life of plastics. However, high temperatures cause the...
The use of degrading enzymes in polymer formulation is a very attractive strategy to manage the end-of-life of plastics. However, high temperatures cause the denaturation of enzymes and the loss of their catalytic activity; therefore, protection strategies are necessary. Once protected, the enzyme needs to be released in appropriate media to exert its catalytic activity. A successful protection strategy involves the use of layered double hydroxides: cutinase, selected as a highly degrading polyester hydrolytic enzyme, is thermally protected by immobilization in Mg/Al layered double hydroxide structures. Different triggering media are here evaluated in order to find the best releasing conditions of cutinase from LDH. In detail, phosphate and citrate-phosphate buffers, potassium carbonate, sodium chloride, and sodium sulfate solutions are studied. After the comparison of all media in terms of protein release and activity retained, phosphate buffer is selected as the best candidate for the release of cutinase from LDH, and the effect of pH and concentration is also evaluated. The amount of the enzyme released is determined with the Lowry method. Activity tests are performed via spectrophotometry.
Topics: Polymers; Hydroxides; Phosphates
PubMed: 36614271
DOI: 10.3390/ijms24010831 -
Acta Cirurgica Brasileira 2023To explore the role and mechanism of curcumin (Cur) in reducing oxidative stress damage in rats with nephrolithiasis induced by ethylene glycol (EG).
PURPOSE
To explore the role and mechanism of curcumin (Cur) in reducing oxidative stress damage in rats with nephrolithiasis induced by ethylene glycol (EG).
METHODS
Thirty male rats were divided into normal control, model, positive (10% potassium citrate), Cur-10 (10 mg/kg curcumin) and Cur-20 (20 mg/kg curcumin) groups.
RESULTS
The results of kidney tissue section stained by hematoxylin-eosin and von Kossa showed that curcumin treatment can inhibit the formation of kidney stones. The biochemical test results showed that the urea (Ur), creatinine (Cr), uric acid (UA), inorganic phosphorus and Ca2+ concentrations in urine decreased after being treated with curcumin. There were significant differences between different doses of curcumin (P < 0.05). Compared with the Cur-10 group, Cur-20 had a more significant inhibitory effect on malondialdehyde (MDA) (P < 0.05). In addition, reverse transcription polymerase chain reaction (PCR) detection and immunohistochemical results indicated that the osteopontin (OPN) in the kidney was significantly reduced after curcumin treatment.
CONCLUSIONS
Curcumin could reduce the oxidative stress damage caused by EG-induced kidney stones.
Topics: Animals; Male; Rats; Antioxidants; Curcumin; Kidney; Kidney Calculi; Osteopontin; Oxidative Stress
PubMed: 37132752
DOI: 10.1590/acb380223 -
Urology Journal Apr 2020This study aimed to investigate the efficacy and safety of febuxostat in patients with radiolucent nephrolithiasis.
PURPOSE
This study aimed to investigate the efficacy and safety of febuxostat in patients with radiolucent nephrolithiasis.
MATERIALS AND METHODS
From March 2016 to June 2018, data of 96 patients with radiolucent nephrolithiasis and hyperuricemia who referred to the Third Affiliated Hospital of Sun Yat-sen University were retrospectively analyzed. These patients were divided into allopurinol 300mg/d (control), febuxostat 40mg/d (F40) and 80mg/d (F80) groups respectively. All patients took potassium citrate as a combination treatment and had been followed up for at least 6 months. Before treatment and on after 1st, 3rd and 6th month, complete blood count, serum uric acid (sUA), hepatic and renal function as well as ultrasound were carried out. Arthritic and gastrointestinal symptoms were also monitored. Computed tomography was performed before treatment and 6 months after medication.
RESULTS
Compared with allopurinol group, F40 group showed no difference in urate-lowering effect, while F80 had the best effect across all the visits (P<0.01). At 6th month, 25(83.3%) cases of F80 group achieved sUA<6mg/ dL, which was better than allopurinol group (18 cases, 58.1%) and F40 group (17 cases, 58.6%). In the dissolution effect of radiolucent calculi, F80 had the best effect, followed by F40 and then allopurinol (P<0.05). No statistical difference was observed in adverse events among three groups.
CONCLUSION
Febuxostat significantly decreased sUA, promoted radiolucent stone dissolution and reduced the total stone number, whereas it did not increase the adverse events.
Topics: Adult; Aged; Allopurinol; Febuxostat; Female; Humans; Hyperuricemia; Male; Middle Aged; Nephrolithiasis; Retrospective Studies; Young Adult
PubMed: 32309869
DOI: 10.22037/uj.v0i0.5564