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At least 19 recordsLinked to original sources
PubMed1999

Action potential conduction block of nerves in vitro by potassium citrate, potassium tartrate and potassium oxalate.

OBJECTIVES: Potassium salts in desensitising formulations are believed to act by blocking nerve conduction. The aim of this study was to assess the ability of some organic potassium salts to block action potential conduction and to compare their effects with potassium chloride and potassium nitrate. MATERIALS AND METHOD: Potassium citrate, oxalate or tartrate were added to Krebs' solutions to raise the potassium concentration to 8-64 mM. The test solutions were applied to rat spinal nerves in a bath while monitoring the compound action potentials evoked by electrical stimulation. RESULTS: All potassium salts attenuated the compound action potential in a dose-dependent manner. There were no significant differences between the effects of potassium tartrate and potassium citrate solutions (p>0.1) which caused significantly greater compound action potential attenuation than the same concentrations of potassium oxalate (p<0.05). On the basis of the potassium ion concentration required to cause 50% attenuation of the compound nerve action potential, the relative potencies of the potassium salts were: citrate = tartrate> oxalate>chloride =nitrate. CONCLUSION: Potassium citrate and potassium tartrate were more effective than other potassium salts in blocking nerve conduction and may be more effective dentinal desensitising agents.

Action Potentials↗
PubMed1987

Effects of sodium citrate, potassium citrate, and citric acid in preventing experimental calcium oxalate urolithiasis in rats.

Male Wistar-strain rats which had been fed a glycolic-acid diet developed severe nephrocalcinosis with urinary calculi within 4 weeks. Rats fed the same diet with citrate salts added had, however, either slight or no nephrocalcinosis without any stones in the urinary system. Nephrocalcinosis intermediate between those in the citrate groups and the glycolic-acid group, with some urinary calculi, was observed in the citric-acid group. During the experiment, the urinary oxalate concentration increased markedly and was higher in the citrate and citric-acid than in the glycolic-acid group. The urinary citrate concentration was significantly higher in the citrate groups and lower in the citric acid and glycolic-acid groups. Therefore, citrate salts can be concluded to inhibit nephrocalcinosis and calculi formation as a result of decreased urinary saturation by means of increase in urinary citrate, in spite of a slight increase in the urinary oxalate.

Animals↗
PubMed1998

Reappraisal of the quantity and nature of renal calcifications and mineral metabolism in the magnesium-deficient rat. Effects of treatment with potassium citrate or the combination magnesium citrate and potassium citrate.

There is an urgent need for drugs capable of inhibiting renal calcifications, nephrocalcinosis and stones included, in humans. Current anticalcification medication is based mainly on alkalinization of the metabolism using potassium-containing citrate alone, despite the fact that calcium stone patients suffer marginally from both magnesium and potassium deficiency. We investigated the anticalcification efficacy of oral potassium citrate versus the combined administration of this drug and magnesium citrate in the magnesium-deficient rat developing corticomedullary nephrocalcinosis and luminal microliths in the long term. Among other things we employed specific stains for calcium and oxalate, light microscopy and element analysis for renal tissue and calcifications, respectively. In addition, minerals in renal tissue, urine and plasma were determined, as well as the state of extracellular calcium homeostasis. Magnesium deficiency caused pure calcium phosphate tissue deposits, containing no magnesium, but no deposition of calcium oxalate in the tubular lumen; tissue magnesium, calcium and phosphorus were increased, and there was marked potassium wastage via urine; despite mild hypercalcemia other signs of hyperparathyroidism were not found. Alkalinization with the two kinds of medication evoked an increase in urinary pH, citrate, and potassium; however, potassium citrate alone tended to aggravate renal concretions, whereas the combination of this drug with magnesium citrate completely prevented concretions. It was concluded that: (1) magnesium deficiency-induced calcifications are oxalate-free and are not sensitive to mobilization by alkalinization with potassium citrate, which might explain the failure of the drug to prevent stone recurrence in clinical stone patients, and (2) the combination of potassium citrate and magnesium citrate, which shows enormous anticalcification efficacy, deserves high priority in clinical trials aimed at evaluating strategies for the prevention of stones.

Animals↗
PubMed1984

Use of potassium citrate as potassium supplement during thiazide therapy of calcium nephrolithiasis.

The effectiveness of potassium citrate as a potassium supplement was compared to that of potassium chloride in 13 patients with calcium nephrolithiasis treated with thiazide. Thiazide treatment alone reduced serum potassium, urinary calcium and citrate without affecting urinary pH. Urinary saturation of calcium oxalate and brushite decreased but not as much as the decrement in urinary calcium because of reduced citrate-calcium complexation. Potassium chloride supplementation averted thiazide-induced hypokalemia and hypocitraturia without influencing hypocalciuric action of thiazide or urinary pH. The decline in urinary saturation of calcium salts paralleled the decrement in urinary calcium. Potassium citrate supplementation also kept urinary calcium low and corrected hypokalemia. Moreover, it increased urinary pH and citrate above levels in other phases. Thus, the ability of thiazide to lower the urinary saturation of calcium oxalate was accentuated by potassium citrate supplementation but not by potassium chloride supplementation, probably owing to increased citrate complexation of calcium. Moreover, the potassium citrate therapy was more effective than potassium chloride supplementation in reducing the propensity for the spontaneous precipitation of calcium oxalate in urine. In conclusion, potassium citrate supplementation may be superior to potassium chloride supplementation in patients receiving thiazide in whom stones form.

Adult↗
PubMed1988

Alkali action on the urinary crystallization of calcium salts: contrasting responses to sodium citrate and potassium citrate.

Alkali therapy is used commonly to prevent recurrent stone formation in patients with distal renal tubular acidosis. We compared the effects of potassium citrate to those of sodium citrate in 6 well defined cases of incomplete distal renal tubular acidosis. The patients were studied during a control phase, during potassium citrate treatment (80 mEq. per day) and during sodium citrate treatment (80 mEq. per day) chosen in random order. Potassium citrate caused a decrease in urinary calcium and a significant increase in urinary citrate that resulted in a significant decrease in the urinary saturation of calcium oxalate. It did not alter the saturation of brushite and sodium urate. However, while sodium citrate also was able to increase the urinary citrate level, there was no decrease in the urinary calcium (owing to the increased sodium load). Thus, the urinary saturation of calcium oxalate did not decrease as much as with potassium citrate and the saturation of brushite increased significantly. Moreover, the urinary saturation of sodium urate increased significantly owing to the enhanced sodium excretion. The results suggest that potassium citrate therapy may retard the crystallization of calcium oxalate and may not cause calcium phosphate crystallization. In contrast, sodium citrate may have no effect or it sometimes may accentuate the crystallization of calcium salts. Thus, our study supports the potential clinical advantage of potassium citrate therapy over sodium alkali treatment in patients with incomplete distal renal tubular acidosis and recurrent calcium nephrolithiasis.

Acidosis, Renal Tubular↗
PubMed1995

[Potassium citrate versus potassium chloride in essential hypertension. Effects on hemodynamic, hormonal and metabolic parameters].

A study was conducted on 25 patients (18 men, seven women; mean age 48 [24-70] years) with essential hypertension (EH) to see whether an increase in potassium supply influences blood pressure as well as metabolic and hormonal parameters, and whether the anion administered together with potassium affects the results. In a randomized, cross-over trial sequence the patients daily received 120 mmol potassium chloride, 120 mmol potassium citrate or a placebo, each for 8 weeks. Between each of the three periods there was a "wash-out" phase of 4 weeks each. After 8 weeks of potassium citrate intake the systolic and diastolic pressures were reduced significantly, by a mean of 6.2/3.8 mm Hg (P < 0.05). But after potassium chloride there was only a small, not significant, reduction. Metabolic and hormonal parameters (fasting glucose concentration, glucose tolerance test, lipid electrophoresis; plasma renin activity, plasma concentration of aldosterone, noradrenaline and insulin) were not significantly changed.--These findings suggest that an increased supply of potassium has a favourable haemodynamic effect, but this varies markedly between different potassium salts. An increase in potassium supply should thus be considered as an additional measure in the treatment of EH. As long as renal function is normal no unfavourable metabolic effect need be feared.

Adult↗
PubMed1984

Augmentation of renal citrate excretion by oral potassium citrate administration: time course, dose frequency schedule, and dose-response relationship.

The time course, dose frequency schedule, and dose-response relationship of the citraturic response to orally administered potassium citrate was examined in 22 normal volunteers and 21 patients with uric acid or calcium nephrolithiasis. The slow-release (wax matrix) preparation of potassium citrate produced a rapid and sustained rise in urinary citrate lasting for up to 12 hours following a single oral administration. Probably owing to this prolonged action, the slow-release preparation when given in a twice-daily or thrice-daily schedule at a dosage of 60 meq or 3.78 Gm citrate/day virtually eliminated the normally wide circadian fluctuation in urinary citrate and maintained urinary citrate at a higher, more constant level throughout the day. The liquid preparation of potassium citrate was less effective in this regard. However, the two preparations of potassium citrate caused an equivalent rise in total 24-hour urinary citrate. When 24-hour excretions of citrate were examined, urinary citrate was shown to reach its peak level by the second day of potassium citrate treatment and to return to the pretreatment level by the second day after the treatment was stopped. The rise in urinary citrate produced by treatment was directly proportional to the dose of potassium citrate. In most hypocitraturic patients with renal stones, potassium citrate 60 meq/day restored normal urinary citrate (greater than 320 mg/day).

Administration, Oral↗
PubMed1994

The effects of sodium citrate and oral potassium citrate on urease-induced crystallization.

OBJECTIVES: To study the effects of citrate on urease-induced crystallization in human urine. MATERIALS AND METHODS: Urine samples were collected from seven healthy volunteers with no history of urinary tract infection or stone disease. Citrate was removed from the urine samples by decomposition with citrate lyase. Citrate was then added to the urine in increasing concentrations. Oral potassium citrate was given to the volunteers and their urine was collected. The samples were incubated with urease and the crystallization induced was observed by the Coulter counter technique, by using an optical microscope and by precipitated material analysis. RESULTS: The initiation of crystallization was markedly delayed by both the addition of citrate to the urine and after the ingestion of citrate. Crystal growth and the resulting precipitation of both calcium and magnesium showed a concentration-dependent reduction when citrate was added up to a concentration of 4 mM. Crystal growth and precipitation of calcium and magnesium were also significantly decreased by oral citrate intake. CONCLUSION: Citrate added to the urine or taken orally markedly delays urease-induced crystallization in human urine.

Administration, Oral↗
PubMed1989

Bioavailability of citrate from two different preparations of potassium citrate.

The bioavailability of citrate from two different preparations of potassium citrate was examined in eighteen normal volunteers during three phases of study. After stabilization on a constant metabolic diet, subjects took a single dose of placebo, "slow-release" potassium citrate tablets (60 meq) or rapid-release liquid potassium citrate preparation (60 meq). Timed urine specimens were collected for 24 hours and analyzed for citrate, potassium, and pH. Similar biochemical findings were observed following administration of the two different preparations with the onset and decline of changes being slightly more rapid for the liquid potassium citrate than the tablet preparation. These equivalent bioavailability data indicate that the liquid preparation is a comparable therapeutic alternative to the tablet form.

Adult↗
PubMed1995

Kaliuresis in normal subjects following oral potassium citrate intake without increased plasma potassium concentration.

Ingestion of potassium salts typically induces both a kaliuresis and an increase in the systemic plasma potassium concentration. In this study normal healthy adults undergoing water diuresis ingested potassium citrate or sodium citrate (0.5 mmol/kg body weight) or continued without ion ingestion (a time control group). Urine was collected over 20-min intervals and venous blood sampled at midinterval. Intake of potassium citrate led to a significant increase in potassium excretion that began during the first postingestion collection and peaked 60-80 min after intake with a maximal increase in potassium excretion above baseline of 1.60 mumol/min.kg-1. The kaliuresis occurred without changes in plasma potassium concentration, excretion of creatinine or calcium, or urine hypo-osmolality and was associated with a briefer, smaller, and less regular increase in sodium excretion and a pronounced but irregular increase in chloride excretion. Plasma aldosterone was insignificantly elevated above baseline, and the initial increase did not occur until 40-60 min after potassium intake. Intake of sodium citrate did not produce a kaliuresis. The cause of the kaliuresis does not appear to be an increased systemic plasma potassium concentration, an increased plasma level of aldosterone, intake of citrate, or an elevated excretion of sodium. The mechanism inducing the kaliuresis following oral potassium intake in the absence of changes in systemic plasma potassium may involve a reflex initiated at potassium sensors in gut, portal vein, or liver.

Administration, Oral↗
PubMed2001

[Therapeutic use of potassium citrate].

Therapeutic indications of potassium citrate include: 1. Oxaluric renal stone disease and some cases of uric acid stone disease. Prevention of stone formation in patients with renal polycystic disease. Prevention of stone relapse after ESWL or lithotomy; 2. Distal renal tubular acidosis complicated by hypercalciuria, mainly in children. 3. Renal hypercalciuria and hyperoxaluria. 4. Prevention of renal complications at the time of glaucoma treatment with acetazolamide. 5. Potassium supplementation during treatment of hypertension. Potassium citrate is usually contraindicated in the case of: 1. Urinary tract infection. 2. Struvite renal stone disease. 3. Hyperpotassemia and advanced chronic renal failure. 4. Peptic ulcer or gastritis. 5. Gastrointestinal bleeding. 6. Disorders of coagulation, crural varices. 7. Metabolic alkalosis. Potassium citrate, when used at therapeutic doses, is to be considered as quite safe. The average daily dose even if admitted as a single dose day engages 60-75% of free renal capacity for potassium excretion. Physiologic and therapeutic citrate concentration in urine exceeds much those available for other inhibitors. The therapeutic dose does not induce any significant changes in any biochemical or endocrine parameter of blood except mild transient metabolic alkalosis. The decrease of urine calcium and increase in oxalate calcium phosphate excretion is observed. In hypo-cytriaturic patients the response to therapeutic dose of citrate is smaller. One-year remission of stone disease is observed in 70-75% cases.

Acetazolamide↗
PubMed1983

Physiological and physiochemical correction and prevention of calcium stone formation by potassium citrate therapy.

Long-term effects of potassium citrate therapy (usually 60 mEq/day) were examined in 53 patients with renal stones (11 with uric acid lithiasis with complication of calcium stones, 10 with hypocitraturia as the sole abnormality, and 28 with hypocitraturia occurring with other abnormalities such as absorptive hypercalciuria, renal tubular acidosis, hyperuricosuric calcium oxalate nephrolithiasis, and enteric hyperoxaluria). Potassium citrate was given alone in 29 patients, added to thiazide and/or allopurinol treatments in 12 patients who continued to form stones on these treatments, and begun concurrently with thiazide and/or allopurinol in 12 patients with hypocitraturia and other defects (hypercalcuria and/or hyperuricosuria). In all three groups of patients, urinary citrate and pH significantly increased during potassium citrate treatment. Urinary saturation of calcium oxalate significantly declined while that of brushite remained unchanged. The propensity for the spontaneous nucleation of calcium oxalate, determined from the minimum amount of added oxalate required to elicit precipitation, declined. The treatment was effective in preventing new stone formation in all three groups. Stone passage rate declined from 5.14-7.41 stones/patient year before potassium citrate treatment to 0.66-1.33 stones/patient year during treatment, and 75.0-91.7% of patients were in remission. In patients who relapsed on other treatments (with passage of 5.14 stones/patient year), the addition of potassium citrate to the ongoing treatment program reduced stone formation to 1.33 stones/patient year and caused remission in 91.7% of patients. In 14 of 33 patients with preexisting radiopaque stones, there was radiological evidence of a reduced number of stones after 8 months-2 years of potassium citrate treatment. In conclusion, potassium citrate restores normal urinary citrate, decreases saturation and propensity for spontaneous nucleation of calcium oxalate, and inhibits new stone formation.

Adult↗
PubMed2002

Prevention of spinal bone loss by potassium citrate in cases of calcium urolithiasis.

PURPOSE: We determine if potassium citrate treatment stabilizes spinal bone density among patients with recurrent calcium oxalate nephrolithiasis. MATERIALS AND METHODS: We studied a group of 16 men and 5 women with stones taking potassium citrate from 11 to 120 months. They represented all patients from the Stone Clinic who took potassium citrate alone for at least 11 months. L2-L4 bone mineral density data before and after potassium citrate treatment were retrieved retrospectively and analyzed. RESULTS: In the combined group L2-L4 bone mineral density increased significantly by 3.1% over mean duration of 44 months. Z score, corrected for age matched normal values, increased significantly by 3.8%. Urinary pH, citrate and potassium increased significantly during treatment but urinary calcium did not change. CONCLUSIONS: Potassium citrate, a commonly used drug for the prevention of recurrent nephrolithiasis, may avert age dependent bone loss. Spinal bone density increased in most patients when it normally decreases.

Adult↗
PubMed1985

Can potassium citrate replace sodium bicarbonate and potassium chloride of oral rehydration solution?

Ninety four children aged less than 5 years with diarrhoeal dehydration and acidosis were treated randomly with either World Health Organisation (WHO) oral rehydration solution containing sodium chloride, potassium chloride, sodium bicarbonate and glucose or an oral solution with tripotassium citrate monohydrate replacing the sodium bicarbonate and potassium chloride in the WHO solution. Fifty five children (58%) were hypokalaemic (potassium less than 3.5 mmol/l) on admission. All but two in the citrate group were successfully treated. There were no significant differences in rehydration solution intake, stool output, gain in body weight, and fall in plasma specific gravity and haematocrit between the two treatment groups after 48 hours' treatment. Significant improvement in the serum potassium concentration was observed in the hypokalaemic children receiving potassium citrate solution compared with children receiving WHO solution after 24 and 48 hours' treatment. None developed hyperkalaemia. Although children receiving potassium citrate solution corrected their acidosis at a slower rate than the WHO solution group during the first 24 hours, by 48 hours satisfactory correction was observed in all. Tripotassium citrate can safely replace sodium bicarbonate and potassium chloride and may be the most useful and beneficial treatment for diarrhoea and associated hypokalaemia.

Acidosis↗
PubMed2001

[Effect of potassium citrate in the prophylaxis of urinary lithiasis].

OBJECTIVE: The physiologic effects of potassium citrate on urinary solubility have led to their use to facilitate stone passage after lithotripsy. The aim of our study is to evaluate the foregoing effects and the efficacy of long-term treatment with potassium citrate to prevent stone recurrence in patients undergoing extracorporeal shock wave lithotripsy. METHODS: A prospective study was conducted on 100 patients with calcium oxalate or calcium phosphate nephrolithiasis that had undergone treatment by extracorporeal shock wave lithotripsy (ESWL). The patients were divided into 4 groups: patients that were stone-free treated with potassium phosphate (25 cases) or fluid diet (25 cases) and patients with persistent residual lithiasis treated with potassium citrate (25 cases) or fluid diet (25 cases). Calculi were classified according to the changes observed during the study compared with the pre-study status as stable (no changes from the pre-study status, with or without residual stone), increased (increase in number or size of the residual stone or recurrence), and decreased (decrease in number or size or passage of the residual stone). RESULTS: Of the 50 patients treated with potassium citrate, 35 (70%) remained stable, 10 cases (20%) showed a decrease and 5 (10%) showed an increase. Of the 50 patients on fluid diet, 19 (38%) remained stable throughout the study, 4 (8%) showed a decrease and 27 (54%) showed an increase in stone size or number. The number of stone recurrence throughout the study in the 100 patients was 25 (25%); of these, 8 were in patients treated with potassium citrate and 17 of those that did not receive potassium citrate. CONCLUSIONS: Potassium citrate therapy has been found to be statistically significantly effective in the control of post-lithotripsy residual stone and stone recurrence.

Adolescent↗
PubMed2002

Dosage of potassium citrate in the correction of urinary abnormalities in pediatric distal renal tubular acidosis patients.

Potassium citrate is an alkaline agent that has been recommended for the prevention of nephrolithiasis in distal renal tubular acidosis (RTA). Information on the effectiveness and the optimal dose of potassium citrate in the correction of urinary abnormalities in pediatric distal RTA is limited, however. We conducted this study to determine the effectiveness and the optimal dose of potassium citrate for the correction of urinary abnormalities and the prevention of nephrolithiasis in children with distal RTA. Eight pediatric distal RTA patients participated in this study. The mean +/- SEM age was 9.7 +/- 1.2 years, and mean body weight was 29.1 +/- 4.7 kg. After initial evaluation, all patients were treated with increasing dosages of potassium citrate starting from 2 mEq/kg/d in three divided doses. The dosage was increased progressively in a stepwise fashion every 2 months from 2 mEq/kg/d to 3 mEq/kg/d, then to 4 mEq/kg/d. Blood and 8-hour overnight urine samples were obtained at baseline and every 2 months before increasing the dosage of potassium citrate. Urinary saturations for calcium oxalate and calcium phosphate were estimated by using Tiselius's indices. The basal urinary calcium-to-creatinine, phosphate-to-creatinine, and calcium-to-citrate ratios and urinary saturation for calcium oxalate and calcium phosphate were elevated significantly, whereas citrate-to-creatinine ratio was reduced significantly in distal RTA patients. These ratios were normalized gradually with the increasing dosage of potassium citrate. All the aforementioned abnormalities were normalized only after the dosage of potassium citrate was raised to 4 mEq/kg/d. The elevation in urinary saturation of calcium phosphate could not be normalized throughout the study, however. These results suggest that 4 mEq/kg/d of potassium citrate supplement can correct successfully most of the urinary abnormalities and the elevated urinary saturation for calcium oxalate but not for calcium phosphate in children with distal RTA. Monitoring of urinary calcium-to-creatinine ratio or citrate-to-creatinine ratio is valuable to ensure adequate potassium citrate supplementation in this group of patients.

Acidosis, Renal Tubular↗
PubMed1997

[Cost-effectiveness analysis of preventive treatment of urinary lithiasis recurrence using potassium citrate].

OBJECTIVE: This study evaluated two possible alternatives of potassium citrate administration-granulate (liquid) and tablet (wax matrix)-versus treatment with diet and/or fluid to prevent recurrence of urinary lithiasis. METHODS: The cost-effectiveness of the alternative modalities were analyzed using data from the studies conducted by Barceló (1993), Pak (1985) and Preminger (1985). The variables utilized for effectiveness were 'avoided relapse' and 'avoided intervention'. Since the data from the foregoing studies did not make any distinction between the two alternative forms of potassium citrate administration, the incidence of side effects and the dropout rate were included. These data were obtained from the studies conducted by Barceló (1993). Campoy (1994) and Conte (1994). RESULTS/CONCLUSION: Potassium citrate is effective in the prevention of recurrence of urinary lithiasis; relapses and interventions were significantly avoided. Both forms of potassium citrate are similarly effective and the only differences found were in regard to the side effects and the dropout rate; however, further studies are warranted to determine the possible differences with more precision. Potassium citrate in granulated form in much more cost-effective than the diet and fluid regimen than the tablet alternative, with a difference significantly in favor of the former in the order of 8:1. Price was the most important variable and therefore it is important to determine the appropriate dosage since it will influence the cost-effectiveness ratio and the allocation of resources.

Clinical Trials as Topic↗