Effect Of Potassium Citrate Research Articles

Anti-urolithiatic effect of Cucumis melo L. var inodorous in male rats with kidney stones.

Melon seed extracts have high antioxidant activities and are effective against a variety of diseases, including kidney stones. In kidney stone model rats, the anti-urolithiatic effects of the hydro-ethanolic extract of melon seed and potassium citrate were studied and compared. After urolithiasis induction by ethylene glycol, the extract and potassium citrate were treated orally for 38days concurrent with ethylene glycol. Then, urine and kidney sampling were done, and the urinary parameter levels were measured. The melon and potassium citrate treatments reduced the kidney index, the levels of urinary calcium and oxalate, calcium oxalate deposit numbers, the score of crystal deposits, histo-pathological damages, and the score of inflammation in the kidney sections, while elevating the urinary pH, magnesium, and citrate levels, and also the expression of the UMOD, spp1, and reg1 genes in the kidney of treated animals. The effect of potassium citrate is the same as the effect of melon in treated animals. So, their effects could be by normalizing urinary parameters, reducing crystal deposits, excreting small deposits from the kidney, reducing the chance of them being retained in the urinary tract, and elevating the expression of the UMOD, spp1, and reg1 genes, which are involved in kidney stone formation.

Comparison of the effects of potassium citrate and hydrochlorothiazide on the ureteral stent encrustation in patients with long stent survival; a single-blinded clinical trial

Introduction: The probability of encrustation after embedding ureteral stent is 9.6% in six weeks, 47.5% in 6 to 12 weeks and 76.3% in more than 12 weeks. Objectives: This study was designed to evaluate the effect of potassium citrate and hydrochlorothiazide on ureteral stent encrustation as a single-blinded clinical trial. Patients and Methods: After embedding ureteral stent in 130 patients, the individuals were randomly divided into two groups using random allocation software. Convenience sampling method was used in this study. One group was given hydrochlorothiazide and potassium citrate, and the other group did not receive any medication. All stents were the same brand and the maximum time of stents being in situ was six weeks. Four to six weeks after stent implantation, patients were referred for stent removal. Then, ureteral stent encrustation was recorded in the two groups according to the visual appearance and the difficulty in stent removing due to stent encrustation. Results: The mean age of the patients was 42.62±14.86 years. Regarding gender, 78 patients (67.8%) were male and 37 patients (32.2%) were female. In this study, 15 patients (13%) had ureteral stent encrustation, of which 13 patients (20%) were in the group without medication and two patients (4%) were in the group who received hydrochlorothiazide and potassium citrate (P = 0.012). Conclusion: The rate of ureteral stent encrustation in the patients who received hydrochlorothiazide and potassium citrate was significantly lower than the patients in the control group. This can be justified by the diuretic properties of hydrochlorothiazide and the reduction of urinary calcium levels. Additionally, high urinary citrate level and induction of urinary alkalization after the administration of potassium citrate. Are the ameliorating factors. Trial Registration: Registration of trial protocol has been approved by Iranian Registry of Clinical Trials (identifier: IRCT20180625040232N3, https://en.irct.ir/trial/46227, ethical code# IR.UMSU. REC.1396.130).

Effect of Potassium Citrate on Cephradine Residues in Broiler Chicks

Effect of Potassium Citrate on Cephradine Residues in Broiler Chicks

Efficient and Facile Fabrication of Hierarchical Carbon Foams with Abundant Nanoscale Pores for Use in Supercapacitors

Hierarchical carbon foams (HCFs) with micro‐, meso‐, and macropores were successfully synthesized via a two‐step process: (1) polymerization in oil‐in‐water (O/W) emulsions without any hard templates and (2) carbonization at 850°C. With the aim of both enhancing the stability of the emulsion and forming a micro‐ and mesoporous structure during the carbonization process, potassium citrate was introduced in an aqueous solution of resorcinol and formaldehyde. A series of HCFs were fabricated by changing the mass ratio of potassium citrate to total carbon sources from 0.25 to 1.5. The effect of potassium citrate on the porous structure of HCFs was investigated through nitrogen sorption tests. The prepared HCFs exhibited well‐developed porous structures of micro‐, meso‐ and macropores and high surface areas. The structural characteristics of the HCFs, including pore size distribution, surface area, and porosity, were significantly dependent on the amount of potassium citrate. It was concluded that potassium citrate greatly contributed to the formation of carbon foams with nano‐sized pore structures and high porosity. Interestingly, it was found that when the mass ratio of potassium citrate to total carbon sources was 0.5, the HCFs showed the highest specific surface area (~1360 m2/g). Furthermore, the capacitive performances of the HCFs were evaluated in a 6.0 M KOH aqueous solution using typical electrochemical methods such as cyclic voltammetry and galvanostatic charge/discharge tests. The capacitance of the HCFs tended to increase with the increase in surface area. In particular, the HCFs with the highest surface area also exhibited excellent electrochemical properties (high capacitance of 224 F/g at 1.0 A/g, high rate capability of 191 F/g at 10.0 A/g). These features may be attributed to both the resulting interconnected pore structure that is easily accessible to ions and the high surface area. We believe that this synthesis strategy can be easily extended to the preparation of hierarchical porous carbon materials with a desirable pore structure by tuning the organic monomer.

The effect of potassium citrate on human primary osteoclasts in vitro

The effect of potassium citrate on human primary osteoclasts in vitro

Effects of potassium citrate or potassium chloride in patients with combined glucose intolerance: A placebo-controlled pilot study

BackgroundExperimental K+ depletion reversibly inhibits insulin secretion, while chronic metabolic acidosis decreases insulin sensitivity. We aimed to investigate the effects of potassium supplementation and alkali supplementation in non-acidotic, normokalemic humans with combined glucose intolerance. Study design and resultsIn this double-blind, placebo-controlled study in 11 subjects (7 male, 4 female, ages 47–63 years), 90meqs of oral KCl or Kcitrate per day for 2weeks each increased insulin production as measured by homeostasis model assessment Beta [KCl=86 (CI 81–91), Kcitrate=88 (82–94), placebo=78 (73–83)%, p<0.04], but only Kcitrate attenuated insulin resistance as assessed by HOMA-IR (insulin resistance, Kcitrate=2.8 (2.5–3.1), placebo=3.2 (2.9–3.5), p<0.03) and only Kcitrate increased quantitative insulin sensitivity check index (Quicki, Kcitrate=0.355 (0.305–0.405), placebo=0.320 (0.265–0.375) p<0.04). These results were confirmed by independent measurements, i.e. HOMA C-peptide and whole body insulin sensitivity index measured during oral glucose tolerance testing. Kcitrate significantly decreased systolic and diastolic 24-hour ambulatory blood pressures (−4.0 (−3 to −5) and −2.7 (−1.9 to −3.5), respectively as compared to placebo, p<0.02) while KCl was without a significant effect. ConclusionsK+ supplementation in the absence of overt K+ depletion improves beta-cell function in subjects with combined glucose intolerance. The insulin-sensitizing and hypotensive effect, however, depend on citrate as the accompanying anion.

Effect of Potassium Citrate on Calcium Phosphate Stones in a Model of Hypercalciuria.

Potassium citrate is prescribed to decrease stone recurrence in patients with calcium nephrolithiasis. Citrate binds intestinal and urine calcium and increases urine pH. Citrate, metabolized to bicarbonate, should decrease calcium excretion by reducing bone resorption and increasing renal calcium reabsorption. However, citrate binding to intestinal calcium may increase absorption and renal excretion of both phosphate and oxalate. Thus, the effect of potassium citrate on urine calcium oxalate and calcium phosphate supersaturation and stone formation is complex and difficult to predict. To study the effects of potassium citrate on urine supersaturation and stone formation, we utilized 95th-generation inbred genetic hypercalciuric stone-forming rats. Rats were fed a fixed amount of a normal calcium (1.2%) diet supplemented with potassium citrate or potassium chloride (each 4 mmol/d) for 18 weeks. Urine was collected at 6, 12, and 18 weeks. At 18 weeks, stone formation was visualized by radiography. Urine citrate, phosphate, oxalate, and pH levels were higher and urine calcium level was lower in rats fed potassium citrate. Furthermore, calcium oxalate and calcium phosphate supersaturation were higher with potassium citrate; however, uric acid supersaturation was lower. Both groups had similar numbers of exclusively calcium phosphate stones. Thus, potassium citrate effectively raises urine citrate levels and lowers urine calcium levels; however, the increases in urine pH, oxalate, and phosphate levels lead to increased calcium oxalate and calcium phosphate supersaturation. Potassium citrate induces complex changes in urine chemistries and resultant supersaturation, which may not be beneficial in preventing calcium phosphate stone formation.

Inhibition of Potassium Citrate on Aggregation of Nano Calcium Oxalate Crystal in Four Different Systems

The effects of potassium citrate (K3cit) on sedimentation and aggregation of 50 nm calcium oxalate dihydrate (COD) crystals was studied in order to explore the mechanism of formation and inhibition of kidney stone. In four different systems, including pure water, urine of healthy person and CaOx stone former before and after taking medicine K3cit, the influences of K3cit on average size (), Zeta potential and optical density of nanoCOD suspensions were studied by nanoparticle size Zeta potential analyzer and ultraviolet spectrophotometer. It was showed that K3cit could specifically adsorb on nanoCOD crystals, and also competed with the inhibitor molecules in urine. Due to the decrease of inhibitors in urine of patients, K3cit can be better to fulfill its inhibitory effect, leading to the largest reduced values of the diameter of COD crystal and the optical density of urine suspension. In conclusion, the inhibitory effect of K3cit on aggregation and sedimentation of calcium oxalate crystals is better in urine of patients, whereas the inhibitory effect has been reduced in urine of control group and patients after taking k3cit.

Effect of Potassium Citrate on Bone Density, Microarchitecture, and Fracture Risk in Healthy Older Adults without Osteoporosis: A Randomized Controlled Trial

The acid load imposed by a modern diet may play an important role in the pathophysiology of osteoporosis. Our objective was to evaluate the skeletal efficacy and safety and the effect on fracture prediction of K-citrate to neutralize diet-induced acid loads. We conducted a randomized, double-blind, placebo-controlled trial at a teaching hospital. Subjects included 201 elderly (>65 yr old) healthy men and women (t-score of -0.6 at lumbar spine). Intervention was 60 mEq of K-citrate daily or placebo by mouth. All subjects received calcium and vitamin D. The primary outcome was change in areal bone mineral density (aBMD) at the lumbar spine by dual-energy x-ray absorptiometry after 24 months. Secondary endpoints included changes in volumetric density and microarchitectural parameters by high-resolution peripheral quantitative computed tomography in both radii and both tibiae and fracture risk assessment by FRAX (Switzerland). K-citrate increased aBMD at lumbar spine from baseline by 1.7 ± 1.5% [95% confidence interval (CI) = 1.0-2.3, P < 0.001] net of placebo after 24 months. High-resolution peripheral quantitative computed tomography-measured trabecular densities increased at nondominant tibia (1.3 ± 1.3%, CI = 0.7-1.9, P < 0.001) and nondominant radius (2.0 ± 2.0%, CI = 1.4-2.7, P < 0.001). At nondominant radius, trabecular bone volume/tissue volume increased by 0.9 ± 0.8%, (CI = 0.1-1.7), trabecular thickness by 1.5 ± 1.6% (CI = 0.7-2.3), and trabecular number by 1.9 ± 1.8% (CI = 0.7-3.1, for all, P < 0.05). K-citrate diminished fracture prediction score by FRAX significantly in both sexes. Among a group of healthy elderly persons without osteoporosis, treatment with K-citrate for 24 months resulted in a significant increase in aBMD and volumetric BMD at several sites tested, while also improving bone microarchitecture. Based on the effect on fracture prediction, an effect on future fractures by K-citrate is possible.

Effects of Potassium Citrate on Irritative Voiding Symptoms of Bladder

Participants will learn that potassium citrate may be a contributor to irritative voiding symptoms.

Clinical Significance of Hypocitraturia in Patients with Nephrolithiasis

Purpose: Hypocitraturia is cited as one of the risk factors promoting stone formation or recurrence of nephrolithiasis. We estimated the relationship between hypocitraturia and other metabolic abnormalities, such as hypercalciuria, hyperuricosuria and hyperoxaluria. The effects of potassium citrate medication were also investigated. Materials and Methods: We selected 706 renal stone patients with hypocitraturia (<320mg/day), who had received extracorporeal shock wave lithotripsy (ESWL) treatment, and examined the relationship between hypocitraturia and other metabolic abnormalities according to sex and age. We also examined the increment effect of urinary citrate and stone-free rate following potassium citrate (Urocitra) medication. Results: Complicated hypocitraturia (coexistence with other metabolic abnormalities) was found in 332 of the 706 patients (47.0%). Of the 706 patients, 242 (34.3%), 112 (15.9%) and 33 (4.7%) had hyperoxaluria, hyperuricosuria and hypercalciuria, respectively. Complicated hypocitraturia was higher in the male than female subjects, and was statistically significant (50.4% vs. 39.8%). In 287 (77%) of the 373 patients who received potassium citrate treatment, the urinary citrate level was increased. The mean urinary citrate level was significantly increased (142.5 vs. 336.2 mg/day) (p<0.01), but the stone free rate was not following the citrate treatment. Conclusions: Potassium citrate was effective in increasing the urinary citrate level. However, prophylactic effects of potassium citrate against recurrent nephrolithiasis must be proved by appropriate comparative studies. (Korean J Urol 2006;47:631-634) ꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏ

Effect of Meal on the Physiological and Physicochemical Actions of Potassium Citrate

The effect of meals on the physiological and physicochemical actions of potassium citrate was examined in 8 patients with nephrolithiasis maintained on a constant metabolic dietary regimen. Potassium citrate (20mEq. 3 times per day), whether given with food or on an empty stomach, significantly increased urinary pH, citrate and potassium, and decreased urinary calcium and ammonium. Moreover, potassium citrate decreased urinary saturation of calcium oxalate and uric acid, although it slightly increased that of brushite. However, there was no significant difference in these measures when the drug was given with meals from the time when it was given on an empty stomach. Thus, the effect of potassium citrate on urinary risk factors is unaffected by food.

Contrasting Effects of Various Potassium Salts on Renal Citrate Excretion*

Mechanisms for the citraturic response to potassium citrate treatment were sought by assessing renal citrate clearance and acid-base status after oral administration of potassium citrate, potassium bicarbonate, and potassium chloride. After 2 weeks of treatment of eight patients with stones at a dose of 80 meq/day, urinary citrate rose significantly from 2.5 +/- 1.6 mmol/day (no drug) to 5.1 +/- 1.7 mmol/day with potassium citrate and to 4.5 +/- 1.5 mmol/day with potassium bicarbonate (P less than 0.05), but did not change significantly with potassium chloride. Citrate clearance increased from 8.0 to 27.4 mL/min with potassium citrate and 25.8 mL/min with potassium bicarbonate (P less than 0.05), but did not increase with potassium chloride. Both potassium citrate and potassium bicarbonate significantly raised urinary bicarbonate and decreased urinary ammonium, titratable acid, and net acid excretion. Potassium chloride was without effect. Effects of potassium citrate on urinary citrate, citrate clearance, and acid-base status tended to be more prominent than those of potassium bicarbonate, but these changes were not significant. Thus, the citraturic action of potassium citrate is largely accountable for by provision of an alkali load. Potassium itself had no effect in the absence of potassium deficiency.