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PubMed1993

Randomized double-blind study of potassium citrate in idiopathic hypocitraturic calcium nephrolithiasis.

In an attempt to document the efficacy of potassium citrate in stone formation, 57 patients with active lithiasis (2 or more stones during the preceding 2 years) and hypocitraturia were randomly allocated into 2 groups, with 1 group taking 30 to 60 mEq. potassium citrate daily in wax matrix tablet formation and the other group receiving placebo. In 18 patients receiving potassium citrate for 3 years stone formation significantly declined after treatment from 1.2 +/- 0.6 to 0.1 +/- 0.2 per patient year (p < 0.0001), in 13 patients (72%) the disease was in remission and all patients showed a reduced stone formation rate individually. In contrast, 20 patients taking placebo medication for 3 years showed no significant change in stone formation rate (1.1 +/- 0.4 to 1.1 +/- 0.3 per patient year) and in only 4 patients (20%) was the disease in remission. The stone formation rate during potassium citrate treatment was significantly lower than during the placebo treatment (0.1 +/- 0.2 versus 1.1 +/- 0.3 per patient year, p < 0.001). Potassium citrate therapy caused a significant increase in urinary citrate, pH and potassium, whereas placebo did not. Adverse reactions to potassium citrate were mild causing only 2 patients in the potassium citrate group and 1 in the placebo group to withdraw from the study. In summary, our randomized trial showed the efficacy of potassium citrate in preventing new stone formation in idiopathic hypocitraturic calcium nephrolithiasis.

Adult↗
PubMed1985

Long-term treatment of calcium nephrolithiasis with potassium citrate.

The long-term effects of potassium citrate therapy (usually 20 mEq. 3 times daily during 1 to 4.33 years) were examined in 89 patients with hypocitraturic calcium nephrolithiasis or uric acid lithiasis, with or without calcium nephrolithiasis. Hypocitraturia caused by renal tubular acidosis or chronic diarrheal syndrome was associated with other metabolic abnormalities, such as hypercalciuria or hyperuricosuria, or occurred alone. Potassium citrate therapy caused a sustained increase in urinary pH and potassium, and restored urinary citrate to normal levels. No substantial or significant changes occurred in urinary uric acid, oxalate, sodium or phosphorus levels, or total volume. Owing to these physiological changes, uric acid solubility increased, urinary saturation of calcium oxalate decreased and the propensity for spontaneous nucleation of calcium oxalate was reduced to normal. Therefore, the physicochemical environment of urine following treatment became less conducive to the crystallization of calcium oxalate or uric acid, since it stimulated that of normal subjects without stones. Commensurate with the aforementioned physiological and physicochemical changes the treatment produced clinical improvement, since individual stone formation decreased in 97.8 per cent of the patients, remission was obtained in 79.8 per cent and the need for surgical treatment of newly formed stones was eliminated. In patients with relapse after other treatment, such as thiazide, the addition of potassium citrate induced clinical improvement. Thus, our study provides physiological, physicochemical and clinical validation for the use of potassium citrate in the treatment of hypocitraturic calcium nephrolithiasis and uric acid lithiasis with or without calcium nephrolithiasis.

Adult↗
PubMed1991

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 (20 mEq. 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.

Adult↗
PubMed1995

Urinary Tamm-Horsfall protein increased after potassium citrate therapy in calcium stone formers.

OBJECTIVES: To evaluate the effect of oral potassium citrate therapy on urinary excretion rates of citrate. Tamm-Horsfall protein (THP), and on calcium oxalate monohydrate crystal agglomeration inhibition [tm], in patients with recurrent calcium stone formation. METHODS: To evaluate the effect of oral therapy with potassium citrate on urinary citrate, THP, and [tm], 24-hour urine samples were collected before and at least 2 months after initiation of oral potassium citrate therapy in 33 calcium stone-forming patients who had no dietary restrictions. The citrate concentration was measured by an adaptation of a citrate lyase method. Urinary disaggregated THP concentration was determined with a quantitative enzyme-linked immunosorbent assay. The [tm] was determined by observing the effects of patients' urine, before and after oral potassium citrate therapy, on the uptake of 45Ca2+ onto the surfaces of added preformed calcium oxalate crystals in a supersaturated solution of calcium oxalate, using the in vitro kinetic method described by other investigators. RESULTS: We observed an increased urinary excretion rate of citrate from a mean of 1.9 mmol/24 h prealkali to 2.6 mmol/24 h postalkali (P < 0.0004) and of THP from a mean of 94.0 mg/24 h prealkali to 199.3 mg/24 h postalkali (P < 0.0016). A corresponding increase in [tm] from a mean of 177.1 minutes prealkali to 221.0 minutes postalkali (P < 0.024) was also observed. CONCLUSIONS: To our knowledge this is the first report correlating increased urinary citrate with THP excretion rate following oral alkalinization with potassium citrate in calcium stone formers. Of clinical importance is the corresponding increase in [tm], which was previously shown to be inversely related to stone-forming activity. Moreover, urinary citrate and THP are known to have a synergistic effect on [tm]. Our data suggest that the effectiveness of potassium citrate therapy in calcium stone-forming patients may, at least in part, be due to increased levels of THP.

Adult↗
PubMed2005

Effect of short-term supplementation of potassium chloride and potassium citrate on blood pressure in hypertensives.

Randomized trials have shown that increasing potassium intake lowers blood pressure. However, most previous trials used potassium chloride, whereas potassium in fruits and vegetables is not a chloride salt. It is unclear whether a nonchloride salt of potassium has a greater or lesser effect on blood pressure compared with potassium chloride. We performed a randomized crossover trial comparing potassium chloride with potassium citrate (96 mmol/d, each for 1 week) in 14 hypertensive individuals. At baseline, blood pressure was 151+/-16/93+/-7 mm Hg with a 24-hour urinary potassium of 81+/-24 mmol. During the randomized crossover part of the study, blood pressure was 140+/-12/88+/-7 mm Hg with potassium chloride (24-hour urinary potassium: 164+/-36 mmol) and 138+/-12/88+/-6 mm Hg with potassium citrate (24-hour urinary potassium: 160+/-33 mmol). These blood pressures were significantly lower compared with that at baseline; however, there was no significant difference in blood pressure between potassium chloride and potassium citrate, mean difference (95% confidence interval): 1.6 (-2.3 to 5.6) mm Hg for systolic and 0.6 (-2.4 to 3.7) mm Hg for diastolic. Our results, in conjunction with the evidence from many previous trials that potassium chloride has a significant blood pressure-lowering effect, suggest that potassium citrate has a similar effect on blood pressure as potassium chloride. These results support other evidence for an increase in potassium intake and indicate that potassium does not need to be given in the form of chloride to lower blood pressure. Increasing the consumption of foods high in potassium is likely to have the same effect on blood pressure as potassium chloride.

Adult↗
PubMed1983

Contrasting effects of potassium citrate and sodium citrate therapies on urinary chemistries and crystallization of stone-forming salts.

Effects of potassium citrate therapy (60 mEq/day) on urinary chemistries and crystallization were compared to those of sodium citrate treatment in five patients with uric acid lithiasis. Both alkali treatments significantly increased urinary pH (P less than 0.001), from 5.35 +/- 0.18 SD to 6.68 +/- 0.14 for potassium citrate and 6.73 +/- 0.20 for sodium citrate. During potassium citrate therapy, urinary calcium significantly declined from 154 +/- 47 mg/day to 99 +/- 23 mg/day (P less than 0.01) and urinary citrate rose from 398 +/- 119 mg/day to 856 +/- 103 mg/day (P less than 0.001). The urinary saturation (activity product ratio) of calcium oxalate decreased from 3.21-fold to 1.69-fold saturation (P less than 0.01), and the inhibitor activity against calcium oxalate precipitation (formation product ratio) significantly increased. However, sodium citrate therapy did not significantly decrease urinary calcium (to 139 +/- 24 mg/day), although it increased urinary citrate substantially (to 799 +/- 89 mg/day, P less than 0.01). Urinary environment became supersaturated with respect to brushite (calcium phosphate) and monosodium urate. The inhibitor activity against calcium oxalate precipitation was not significantly altered for the whole group; in two patients, it decreased by more than 30%. The results indicate that (1) both alkali therapies are equally effective in preventing uric acid stone formation because of their ability to increase urinary pH, and (2) potassium citrate may prevent the complication of calcium nephrolithiasis in patients with uric acid stones, whereas sodium citrate may not.

Adult↗
PubMed1986

Urinary response to oral potassium citrate therapy for urolithiasis in a private practice setting.

Oral potassium citrate therapy was recently approved for treatment of urolithiasis based on results of experiments in a university research setting. However, no supporting studies from private practice have been published. The present study was undertaken to assess the response to one week of oral potassium citrate therapy (60 mEq/day), with respect to urinary risk factors for kidney stones, in a private practice setting. A significant rise in urinary pH, citrate, and potassium excretion, accompanying a significant fall in calcium excretion, were observed. Urinary saturation of calcium oxalate was significantly reduced, as some risk factors in urolithiasis were corrected with oral potassium citrate therapy. The response to therapy in private practice was comparable to that observed in a university research setting.

Adolescent↗
PubMed2001

A comparison of the effects of potassium citrate and sodium bicarbonate in the alkalinization of urine in homozygous cystinuria.

For many years, urine alkalinization has been one of the cornerstones in the treatment of homozygous cystinuria. Because of the relationship found between the excretion of urinary sodium and cystine, potassium citrate has emerged as the preferred sodium-free alkalizing agent. To evaluate the usefulness of potassium citrate for urine alkalization in cystinuric patients, sodium bicarbonate and potassium citrate were compared in 14 patients (10 on tiopronin treatment and four without treatment with sulfhydryl compounds). The study started with 1 week without the use of any alkalizing agents (Period 0) followed by 2 weeks with sodium bicarbonate (Period 1) and 2 weeks with potassium citrate (Period 2). Urinary pH, volume, excretion of sodium, potassium, citrate and free cystine, as well as the plasma potassium concentration, were recorded. Potassium citrate was shown to be effective as an alkalizing agent and, in this respect, not significantly different from sodium bicarbonate. Even though a normal diet was used, a significant increase in urinary sodium excretion was observed with sodium bicarbonate (Period 1). Urinary potassium and citrate excretion increased with potassium citrate (Period 2). A significant correlation was found between urinary sodium and cystine in the tio-pronin-treated patients. No significant differences in cystine excretion were recorded in Periods 0, 1 and 2. Plasma potassium was significantly higher during Period 2, but only one patient developed a mild hyperkalemia (5.0 mmol/l). The use of potassium citrate for urine alkalization in homozygous cystinuria is effective and can be recommended in the absence of severe renal impairment.

Adult↗
PubMed1975

The mechanism of myocardial damage following potassium citrate (Melrose) cardioplegia.

To determine the reasons for clinical failure of Melrose solution, potassium arrest was studied in isolated working rat hearts. Eight control hearts were stable for 2-1/2 hours. After 1/2 hour of work, 42 experimental hearts were subjected to 1 hour of ischemis by aortic cross-clamping with unmodified ischemia in eight hearts and ischemia with simultaneous intracoronary injection of 5 ml. of 4 degrees C. (1)Krebs-Henseleit buffer in seven hearts (2)potassium chloride buffer in six hearts, (3)potassium citrate buffer in eight hearts (both 26 mEq. per liter of K, approximately 300 mOsm. per liter), (4)Melrose solution in seven hearts (greater than 200 mEq. per liter of K, greater than 400 mOsm. per liter), (5)hypertonic potassium citrate buffer in six hearts (26 mEq. per liter of K, greater than 400 mOsm. per liter). The pH of all solutions was 7.8 plus or minus 0.1. After recovery isotonic potassium citrate- and potassium chloride-arrested hearts and time-matched control hearts showed no significant differences in cardiac output, coronary flow, systolic pressure, or heart rate. Hypertonic potassium citrate decreased the recovery of cardiac function after arrest and Melrose arrest was not significantly different from unmodified ischemia. Intracoronary cold isotonic Krebs-Henseleit buffer was better than Melrose arrest but inferior to 26 mEq. er liter of potassium arrest. Arrest with 26 mEq. per liter of potassium augments perfusion hypothermia and prevents significant functional and histologic myocardial damage during 1 hour of ischemis. Previous authors assumed that hypertonicity and citrate were responsible for poor results with Melrose solution, but high potassium concentration is the major deleterious factor with hypertonicity playing a contributory role.

Animals↗
PubMed2000

Effects of dietary potassium citrate supplementation on urine pH and urinary relative supersaturation of calcium oxalate and struvite in healthy dogs.

OBJECTIVE: To assess the effect of dietary potassium citrate supplementation on the urinary pH, relative supersaturation of calcium oxalate and struvite (defined as the activity product/solubility product of the substance), and concentrations of magnesium, ammonium, phosphate, citrate, calcium, and oxalate in dogs. ANIMALS: 12 healthy adult dogs. PROCEDURE: Canned dog food was fed to dogs for 37 days. Dogs were randomly allocated to 3 groups and fed test diets for a period of 8 days. Study periods were separated by 6-day intervals. During each study period the dogs were fed either standard diet solus (control) or standard diet plus 1 of 2 types of potassium citrate supplements (150 mg potassium citrate/kg of body weight/d) twice daily. Urinary pH, volume and specific gravity, relative supersaturation of calcium oxalate and struvite, and concentrations of magnesium, ammonium, phosphate, calcium, oxalate, and citrate were assessed for each treatment. RESULTS: Mean urine pH was not significantly affected by dietary potassium citrate supplementation, although urine pH did increase by 0.2 pH units with supplementation. Diets containing potassium citrate maintained a higher urine pH for a longer part of the day than control diet. Three Miniature Schnauzers had a significantly lower urinary relative calcium oxalate supersaturation when fed a diet supplemented with potassium citrate, compared with control diet. CONCLUSIONS AND CLINICAL RELEVANCE: Dietary potassium citrate supplementation has limited effects on urinary variables in most healthy dogs, although supplementation results in maintenance of a higher urine pH later in the day. Consequently, if supplementation is introduced, dogs should be fed twice daily and potassium citrate should be given with both meals or with the evening meal only.

Animals↗
PubMed2002

Potassium citrate prevents increased urine calcium excretion and bone resorption induced by a high sodium chloride diet.

The amount of sodium chloride in the diet of industrialized nations far exceeds physiological requirements. The impact of abundant dietary salt on skeletal health has yet to be established, but is potentially detrimental through increased urinary calcium losses. We examined the effect of increased dietary sodium chloride on urine calcium excretion and bone turnover markers in postmenopausal women and, further, whether potassium citrate attenuates the effects of increased dietary salt. Postmenopausal women (n = 60) were adapted to a low-salt (87 mmol/d sodium) diet for 3 wk, then randomized to a high-salt (225 mmol/d sodium) diet plus potassium citrate (90 mmol/d) or a high-salt diet plus placebo for 4 wk. Urine calcium, urine N-telopeptide, urine cAMP, serum osteocalcin, and fasting serum PTH were measured at the end of the low- and high-salt diets. On the high salt plus placebo diet, urine calcium increased 42 +/- 12 mg/d (mean +/- SEM), but decreased 8 +/- 14 mg/d in the high salt plus potassium citrate group (P = 0.008, potassium citrate vs. placebo, unpaired t test). N-telopeptide increased 6.4 +/- 1.4 nanomoles bone collagen equivalents per millimole creatinine in the high salt plus placebo group and 2.0 +/- 1.7 nanomoles bone collagen equivalents per millimole creatinine in the high salt plus potassium citrate group (P < 0.05, potassium citrate vs. placebo, unpaired t test). Osteocalcin, PTH, and cAMP were not significantly altered. The addition of oral potassium citrate to a high-salt diet prevented the increased excretion of urine calcium and the bone resorption marker caused by a high salt intake. Increased intake of dietary sources of potassium alkaline salts, namely fruit and vegetables, may be beneficial for postmenopausal women at risk for osteoporosis, particularly those consuming a diet generous in sodium chloride.

Aged↗
PubMed1994

[Granulated potassium citrate in the prevention of calcium oxalate lithiasis].

Since the approval of potassium citrate for the treatment of urolithiasis, there are many patients in other countries who have benefited from this drug. This paper describes the biochemical changes and tolerance seen in fifteen patients treated for one month with granulated potassium citrate. Some significant changes are observed in serum potassium and creatinine, and in urinary pH, citrate and potassium. Tolerance was good. Our results confirm that potassium citrate is an effective, easy to use, and well tolerated drug for the prophylaxis of oxalocalcium lithiasis.

Calcium Oxalate↗
PubMed1985

Prevention of recurrent calcium stone formation with potassium citrate therapy in patients with distal renal tubular acidosis.

Distal renal tubular acidosis is a common cause of intractable calcium nephrolithiasis. We examined the effect of oral potassium citrate therapy in 9 patients with incomplete distal renal tubular acidosis diagnosed on the basis of an abnormal response to an oral ammonium chloride load. Patients were studied during a control phase and after 3 months of potassium citrate treatment (60 to 80 mEq. daily). Potassium citrate caused a significant increase in urinary pH and urinary citrate, and a decrease in urinary calcium. The urinary relative saturation ratio of calcium oxalate significantly decreased during treatment, while that of brushite did not change. Potassium citrate also was shown to inhibit new stone formation. During a mean treatment period of 34 months none of the 9 patients had new stones, although 39.3 plus or minus 79.7 (standard deviation) stones per patient formed during the 3 years preceding treatment. The results support the potential clinical advantage of potassium citrate therapy in patients with distal renal tubular acidosis and recurrent calcium nephrolithiasis.

Acidosis, Renal Tubular↗
PubMed2003

Long-term combined treatment with thiazide and potassium citrate in nephrolithiasis does not lead to hypokalemia or hypochloremic metabolic alkalosis.

BACKGROUND: Potassium citrate is commonly used in combination with a thiazide diuretic in the medical management of recurrent hypercalciuric nephrolithiasis. However, concerns have been raised that administration of this nonchloride potassium alkali with a kaliuretic and natriuretic agent such as thiazide may not be efficacious in correcting or preventing hypokalemia, and may produce hypochloremic metabolic alkalosis. This retrospective analysis was conducted to determine if these two potential complications are encountered in patients on long-term potassium citrate and thiazide therapy. METHODS: Data were collected on 95 patients who had been on combination therapy for at least 4 months from the stone clinics of the University of Texas Southwestern Medical Center, Duke University Medical Center, and Ochsner Clinic. RESULTS: Mean serum potassium concentration remained within normal limits without a significant decrease during combined therapy. Serum chloride was significantly lower from pretreatment but by only 1 mEq/L and remained within normal limits throughout treatment. There was a small increase in serum bicarbonate concentration compared to the baseline level of less than 1 mEq/L at 8 to 12 and 18 to 24 months, but not at other treatment periods. CONCLUSION: Co-administration of potassium citrate did not induce hypokalemia or hypochloremic metabolic alkalosis in our thiazide-treated patient population.

Adolescent↗
PubMed2002

Oral potassium citrate treatment for idiopathic hypocitruria in children with calcium urolithiasis.

PURPOSE: We evaluated the clinical and laboratory outcome of oral potassium citrate treatment in children with idiopathic hypocitruria and calcium stones. MATERIALS AND METHODS: The charts of 64 children 1 to 15 years old with hypocitruria and calcium stones (median age 7.2) treated with oral potassium citrate were reviewed. Evaluation parameters were tolerability, adverse reactions, metabolic profile and stone recurrence. RESULTS: No serious adverse reaction due to potassium citrate administration was recorded. Normal citrate excretion was restored in all patients. After treatment median urinary citrate daily plus or minus SD increased from 197 +/- 72 to 632 +/- 218 mg./1.73 m.2 (p <0.001) and mean urinary pH increased from 5.3 +/- 0.3 to 6.2 +/- 0.7 (p <0.01). Mean calcium excretion decreased from 3.5 +/- 2.7 to 2.5 +/- 2.7 mg./kg. (p <0.05). At an average followup of 22 months (range 3 to 67) the recurrence rate in the group overall was 0.07 per patient-year. The previous recurrence rate of 0.32 per patient-year in the 20 children with a history of recurrent stone disease decreased to 0.17 per patient-year after treatment. None of the 44 initial stone formers had recurrent stones. CONCLUSIONS: Our results show the safety and efficacy of oral potassium citrate treatment for restoring normal urinary citrate and suggest a preventive effect for recurrent calcium stone disease in children with hypocitruria and calcium stones.

Administration, Oral↗
PubMed1992

[Clinical study of Urocit-K: a slow releasing potassium citrate].

Citrate is recognized as one of the inhibitors of urinary stone formation. If the urinary citrate and pH could be elevated by the supply of potassium citrate, the recurrence of stone formation would hopefully be prevented. Urocit-K is a kind of slow releasing preparation of potassium citrate. The pharmacokinetics of Urocit-K is investigated in this study, which included two groups: 1) the hypocitraturia group consisting of twenty patients and 2) the normal volunteer group consisting of ten persons. Urokit-K was administered to patients in 10 mEq doses, t.i.d. for 2 weeks. Comparison of urinary biochemistry was done prior to, and one week after administration of the Urocit-K. In the normal volunteer group, the pharmacokinetics of Urocit-K was determined by urinary pH, K, and citrate. Determinations were made six times a day (every 2-hours for first 8 hours, 7- and 9- hours for the last 16 hours) with Urocit-K for comparison. This study indicated that Urocit-K increases urinary pH, K, and citrate in hypocitraturic patients. In the normal volunteer group, Urocit-K deserves its slow-releasing property shown by a constant increase of urinary pH and K for the first 8 hours; and urinary citrate for almost 24 hours. No apparent complications, such as gastrointestinal upset or cardiopulmonary discomfort were observed. In conclusion, Urocit-K is an excellent preparation of potassium citrate and a good choice for prevention of stone recurrence.

Citrates↗
PubMed2006

Effect of potassium citrate therapy on stone recurrence and regrowth after extracorporeal shockwave lithotripsy in children.

BACKGROUND AND PURPOSE: Stone disease in children may cause functional and morphologic changes in the urinary tract during longer-term follow-up. Prevention of stone recurrence will be possible only with careful metabolic evaluation and appropriate management. The possible preventive effects of potassium citrate therapy on true stone recurrence, as well as regrowth rates after shockwave lithotripsy (SWL), were evaluated in children treated for renal stones. PATIENTS AND METHODS: Following assessment of the efficacy of SWL, 96 children (72 male, 53 female aged 4 to 14 years with a mean of 6.6 years) were evaluated for the effects of potassium citrate on residual fragments as well as true new stone formation during long-term follow-up. All children had calcium-containing stones with normal renal morphology and function without any urinary-tract infection. Depending on the outcome of treatment, patients with and without residual stones were allocated independently to Group I (N = 52) and Group II (N = 44), which were matched for sex and age. Group I was given oral potassium citrate 1 mEq/kg daily for 12 months; the remaining children served as controls. Follow-up ranged from 12 to 36.6 months, with a mean of 24.4 months. Follow-up results for at least a year with respect to the stone recurrence or stone growth rates were recorded in both groups. RESULTS: Stone-free children undergoing no specific therapy had significant new stone formation compared with the group receiving potassium citrate on a regular basis (34.6% and 7.6%, respectively). Children with residual fragments receiving no specific preventive measure also showed significant new stone formation, along with enlargement of the fragments. CONCLUSION: In addition to stone removal, treatment of pediatric urolithiasis requires a thorough metabolic evaluation. Depending on the abnormalities, each patient should be advised on adequate drinking to increase the urine volume in accordance with body size. Although children with hypocitraturia may well benefit from therapeutic agents that raise the urine citrate concentration, our results did clearly show that all children bearing residual fragments should be counseled on adequate fluid intake along potassium citrate treatment to prevent stone regrowth or formation during long-term follow-up.

Adolescent↗
PubMed1986

Idiopathic hypocitraturic calcium-oxalate nephrolithiasis successfully treated with potassium citrate.

The effects of long-term treatment with potassium citrate, 30 to 80 meq/d over 2.13 +/- 0.76 (SD) years, were examined in 37 patients with "idiopathic" hypocitraturic calcium-oxalate nephrolithiasis, in whom the main causes of hypocitraturia (renal tubular acidosis, chronic diarrhea, urinary tract infection, or hypokalemia) were excluded or considered unlikely. Potassium citrate treatment produced a sustained increase in urinary citrate excretion from initially low values (223 to 253 mg/d) to within normal limits (470 to 620 mg/d). Urinary pH rose significantly and was maintained at 6.5 to 7.0. Along with these changes, urinary saturation of calcium oxalate declined significantly to normal limits. Further stone formation ceased in 89.2% of patients during treatment, and the stone formation rate declined from 2.11 +/- 5.68 to 0.28 +/- 1.30 stones/patient-year (p less than 0.01).

Adult↗