SEARCH · PubMed Health

Results for “Potassium Citrate”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 55 records · Page 3Linked to original sources

PubMed2002

Effect of potassium citrate therapy on stone recurrence and residual fragments after shockwave lithotripsy in lower caliceal calcium oxalate urolithiasis: a randomized controlled trial.

BACKGROUND AND PURPOSE: To evaluate the efficacy of potassium citrate treatment in preventing stone recurrences and residual fragments after shockwave lithotripsy (SWL) for lower pole calcium oxalate urolithiasis. PATIENTS AND METHODS: One hundred ten patients who underwent SWL because of lower caliceal stones and who were stone free or who had residual stone 4 weeks later were enrolled in the study. The average patient age was 41.7 years. All patients had documented simple calcium oxalate lithiasis without urinary tract infection and with normal renal morphology and function. Four weeks after SWL, patients who were stone free (N = 56) and patients who had residual stones (N = 34) were independently randomized into two subgroups that were matched for sex, age, and urinary values of citrate, calcium, and uric acid. One group was given oral potassium citrate 60 mEq per day, and the other group served as controls. RESULTS: In patients who were stone free after SWL and receiving medical treatment, the stone recurrence rate at 12 months was 0 whereas untreated patients showed a 28.5% stone recurrence rate (P < 0.05). Similarly, in the residual fragment group, the medically treated patients had a significantly greater remission rate than the untreated patients (44.5 v 12.5%; P < 0.05). CONCLUSION: Potassium citrate therapy significantly alleviated calcium oxalate stone activity after SWL for lower pole stones in patients who were stone free. An important observation was the beneficial effect of medical treatment on stone activity after SWL among patients with residual calculi.

Adolescent↗

PubMed1997

Chronopharmacological studies on potassium citrate treatment of oxalocalcic urolithiasis.

The effect of minimum doses of extradietary potassium citrate ingestion on urolithogenic parameters has been studied. Separate urine fractions were collected in 24-hour periods. Five calcium oxalate stone formers have participated in the study. pH, calcium, citric acid, and the crystallization inhibitory capacity levels in fractional urine samples were determined before and during treatment. The most beneficial effect (increase in citraturia and crystallization inhibitory capacity) was produced by potassium citrate tablets ingested after dinner.

Adult↗

PubMed1985

Comparative efficacy of "specific" potassium citrate therapy versus conservative management in nephrolithiasis of mild to moderate severity.

It generally is believed that conservative measures of high fluid intake and dietary modification in the setting of a stone clinic could favorably influence the course of renal stone disease. To establish the effect of specific medical treatment from the stone clinic effect, we compared the results of potassium citrate therapy to those of 11 reported conservative or placebo trials. The 54 patients receiving potassium citrate chosen for this comparison had mild to moderately severe stone disease (less than 1 stone per patient per year), similar to that encountered in conservative placebo trials (mean 0.54 stones per patient per year). New stone formation was virtually eliminated by potassium citrate therapy (a decrease from 0.52 to 0.02 stones per patient per year, a remission rate of 96 per cent, p less than 0.001), whereas it continued in 39 per cent of the patients during conservative or placebo trials. However, in patients participating in conservative or placebo trials new stone formation decreased by only 54 per cent (from 0.54 to 0.25 stones per patient per year). The superior response to potassium citrate suggested that this specific medical treatment exerted an additional favorable effect on the course of stone disease above the stone clinic effect.

Citrates↗

PubMed2000

Cross-over study of the influence of bicarbonate-rich mineral water on urinary composition in comparison with sodium potassium citrate in healthy male subjects.

Urine volume is the greatest risk factor for nephrolithiasis. High fluid intake is the first general advice given to stone-forming patients for the prevention of their recurrence. The aim of the present study was to evaluate the influence of bicarbonate-rich mineral water (1715 mg bicarbonate/l) on urinary-stone risk factors in comparison with sodium potassium citrate, a well-established treatment for urinary stones. The mineral water and sodium potassium citrate were administered in equimolar concentrations, with respect to the alkali load. All investigations were carried out in healthy male subjects aged 23-38 years. The study followed a cross-over design. All subjects received a standardized diet during the cross-over phase, which was formulated according to the dietary recommendations of the German Society of Nutrition (Deutsche Gesellschaft für Ernährung, 1996). On the loading day of the cross-over phase, fruit tea was substituted for either mineral water or sodium potassium citrate dissolved in fruit tea. The treatment offered during the second part of the cross-over phase was continued for a 4-week follow-up under normal dietary conditions. During the cross-over phase, there was a significant increase in urinary pH (p < 0.001). There was also a significant increase in the excretion of citric acid (P < 0.01), a decrease in the excretion of oxalic acid, and therefore a decrease in the relative supersaturations for calcium oxalate and uric acid. In the follow-up phase also, the relative supersaturations decreased and there were beneficial effects on the other urinary variables. The effect of the bicarbonate-rich mineral water was similar to that of the sodium potassium citrate, which suggests that it could be useful in the prevention of the recurrence of calcium oxalate and uric acid stones.

Adult↗

PubMed1991

Inhibition by sodium-potassium citrate (CG-120) of calcium oxalate crystal growth on to kidney stone fragments obtained from extracorporeal shock wave lithotripsy.

Retention of fragments within the kidney after extracorporeal shock wave lithotripsy (ESWL) continues to be a major shortcoming of this form of stone treatment. The aim of this study was to evaluate the ability of sodium-potassium citrate to inhibit calcium oxalate crystal nucleation and growth on to stone fragments remaining after ESWL. The continuous flow crystallisation technique was adapted to induce calcium oxalate crystal nucleation and growth on to the surface of fragmented kidney stones and the inhibitory effect of sodium-potassium citrate was assessed by scanning electron microscopy and by determining the relative increase in crystalline mass at final concentrations of 0, 2, 4, 6, 8, 10 mmol/l. Sodium-potassium citrate significantly inhibited the deposition of new crystalline calcium oxalate in a dose-dependent manner above 2 mmol/l; these findings were confirmed by scanning electron microscopy. It was concluded that sodium-potassium citrate may provide an effective means of preventing the formation of new kidney stones by the deposition of calcium oxalate on to residual stone fragments resulting from ESWL and that the technique used is an efficient means of testing the efficacy of therapeutic agents to prevent stone recurrence in patients treated with ESWL.

Calcium Oxalate↗

PubMed1993

Study of potassium citrate treatment of crystalluric nephrolithiasis.

Patients with crystalluric nephrolithiasis were treated orally with aqueous potassium citrate solution three times a day with a large quantity of water. After administration of potassium citrate, citric acid (P < 0.001) and potassium (P < 0.001) excretion was significantly increased. Increase in protein (P < 0.05) and uric acid (P < 0.05) excretion in urine revealed their association with the crystallization process. Crystals were absent in 12 (71%) out of 17 patients. Calcium excretion in urine was significantly decreased (P < 0.05). A decrease of calcium ions availability to oxalate ions to form calcium oxalate crystals may result in the prevention of calcium oxalate stone formation.

Adult↗

PubMed2004

Effects of potassium citrate supplementation on bone metabolism.

Western diets rich in animal protein result in long-term acid loading that, despite corresponding increases in net renal acid excretion, may induce a chronic state of acidemia. This may have deleterious effects on both the kidney and bone, by increasing the risk of calcium stone in the former and leading to chemical dissolution of mineral alkaline salts in the latter. Whereas supplementation with alkaline citrate has been shown to reduce stone recurrences, its effect on bone turnover has received less attention. The aim of the present study was to evaluate whether potassium citrate favorably affects bone turnover markers in postmenopausal females with low bone density. Thirty women, aged 58 +/- 8.1 years, were enrolled and studied on basal conditions and after a 3-month course of potassium citrate supplementation (0.08-0.1 g/kg b.w. daily). Twenty-two women concluded the study while 8 withdrew. Twenty-four age-matched healthy women were taken as control cases. All were evaluated for electrolyte and acid-base balance-related parameters, bone turnover, markers and renal function. A significant decrease in net acid excretion was observed upon citrate supplementation, and this was paralleled by a significant decrease of urinary deoxypyridinolines, hydroxyproline-to-creatinine ratios, and, to a lesser extent, serum osteocalcin. Percent variations of urine citrate were inversely related to those of deoxypyridinolines and hydroxyproline. No change in these chemistries occurred in the control group. Our results suggest that treatment with an alkaline salt, such as potassium citrate, can reduce bone resorption thereby contrasting the potential adverse effects caused by chronic acidemia of protein-rich diets.

Absorptiometry, Photon↗

PubMed1996

Long-term effects of potassium citrate therapy on the formation of new stones in groups of recurrent stone formers with hypocitraturia.

OBJECTIVE: To compare stone formation rates before (as total rates and during remote periods) and after therapy with potassium citrate in patients with hypocitraturia. PATIENTS AND METHODS: The study comprised 15 patients with hypocitraturia only (Group I) and 12 patients with hypocitraturia associated with other abnormalities (Group II), all of whom were recurrent stone formers. Their urine chemistry, including citrate, was measured before and after treatment. RESULTS: In both groups, the urinary citrate concentration increased significantly to within normal limits during therapy with potassium citrate (P < 0.005). The rate of total stone formation in patients in Group I decreased significantly from 0.7/year before to 0.13/year after treatment (P < 0.005). The corresponding remote stone formation rate before (0.88/year) was significantly greater than the rate after treatment (0.13/year; P < 0.005; follow-up 4.6 +/- 1.9 years). Patients in Group II showed a similar striking decrease in total stone formation rate, from 1.2/year to 0.08/year after treatment (P < 0.005). The corresponding remote stone formation rate (1.66/year) before was significantly greater than that after treatment (0.08/year; P < 0.005; follow-up 4.1 +/- 1.6 years). There was a remission rate of 93% for stone formation over the complete follow-up. CONCLUSION: Potassium citrate appears to be the drug of choice in the long-term treatment of patients with hypocitraturia as it not only decreases the rate of stone formation but also maintains normal citrate levels in the urine.

Administration, Oral↗

PubMed1985

Correction of hypocitraturia and prevention of stone formation by combined thiazide and potassium citrate therapy in thiazide-unresponsive hypercalciuric nephrolithiasis.

Thirteen patients with hypercalciuric calcium nephrolithiasis continued to form calcium stones when treated with thiazide (4.69 +/- 6.62 [mean +/- SD] stones per patient-year to 5.12 +/- 10.87 stones per patient-year), despite adequate hypocalciuric response (a reduction in urinary calcium levels from 303 +/- 119 mg per day to 193 +/- 88 mg per day, p less than 0.01). Because they had hypocitraturia (250 +/- 86 mg per day versus 643 +/- 236 mg per day in normal subjects, p less than 0.001), potassium citrate (10 to 20 meq three times per day) was added to the ongoing treatment program. During combined treatment with thiazide and potassium citrate, urinary pH significantly rose, and normal levels of urinary citrate were restored. Ten patients stopped forming new stones and all 13 had reduced stone formation rate. Thus, potassium citrate supplementation should be considered in patients requiring thiazide therapy for the control of hypercalciuric nephrolithiasis, especially if they have concurrent hypocitraturia or if it develops during thiazide therapy.

Adult↗

PubMed2004

Comparative investigation of the desensitizing efficacy of a new dentifrice containing 5.5% potassium citrate: an eight-week clinical study.

OBJECTIVE: This double-blind clinical study was designed to investigate the relative effectiveness of a new desensitizing test dentifrice containing 5.5% potassium citrate, 1.14% sodium monofluorophosphate (MFP) and 10% high-cleaning silica (HCS) in a silica base for reducing dentinal hypersensitivity over an eight-week period, to that of a commercially available desensitizing positive control dentifrice containing 3.75% potassium chloride, 0.32% sodium fluoride and 0.3% triclosan in a silica base. METHODOLOGY: A total of 80 subjects were entered into the study, and stratified into two balanced groups according to their baseline mean thermal (air blast) and baseline mean tactile (Yeaple Probe) sensitivity scores. The two groups were randomly assigned to use either the test dentifrice containing potassium citrate/MFP/HCS, or the positive control dentifrice containing potassium chloride/sodium fluoride/triclosan. The two groups were well balanced with regard to their mean baseline thermal and tactile sensitivity scores, sex and age. Subjects were instructed to brush their teeth twice daily (morning and evening) for one minute with their assigned dentifrice and a commercially available soft-bristled toothbrush. Dentinal hypersensitivity examinations, which included tactile sensitivity and thermal sensitivity, were conducted at baseline, four weeks, and eight weeks. Examinations were conducted by the same dental examiner on the subjects at each examination. RESULTS: After four weeks' use of their assigned products, those subjects in the test dentifrice group demonstrated no statistically significant difference for controlling dentinal hypersensitivity as compared to the positive control dentifrice group in tactile and air blast. After eight weeks' use of their assigned products, those subjects in the test dentifrice group again demonstrated no statistically significant difference in tactile and air blast sensitivity as compared to the positive control dentifrice group. CONCLUSION: The results of this double-blind clinical study indicate that the use of a commercially available test dentifrice containing 5.5% potassium citrate, 1.14% sodium monofluorophosphate and 10% high-cleaning silica in a silica base demonstrates no statistically significant difference in tactile and air blast sensitivity compared to the commercially available desensitizing positive control dentifrice containing 3.75% potassium chloride, 0.32% sodium fluoride and 0.3% triclosan in a silica base.

Dentifrices↗

PubMed2004

Renal tubular cell damage and oxidative stress in renal stone patients and the effect of potassium citrate treatment.

Our objective was to evaluate the oxidative stress and renal tubular cell damage in patients who have renal stones compared to normal subjects. The patients were re-evaluated after 1-months supplementation with potassium citrate. We recruited 30 patients (11 males and 19 females) diagnosed with kidney stones and scheduled for surgical stone removal the following month, and 30 healthy non-stone formers (14 males and 16 females). Two 24-h urine samples and one heparinized blood sample were collected from each subject. Plasma was separated from the erythrocytes and assayed for creatinine, potassium, sodium, calcium, magnesium, phosphate, malondialdehyde (MDA, a lipid peroxidation product) (P-MDA), protein thiol as an indicator of protein oxidation, and vitamin E. Erythrocytes were analysed for MDA (E-MDA), reduced glutathione (GSH) and cellular glutathione peroxidase (cGPx) activity. The urine was analyzed for pH, creatinine, potassium, sodium, calcium, magnesium, phosphate, oxalate, citrate, MDA (U-MDA), total protein (U-protein) and N-acetyl-beta-glucosaminidase (NAG) activity. For the stone patients, urine and blood samples were re-evaluated after supplementation with potassium citrate (60 mEq/day) for 1 month. Renal stone patients had higher plasma creatinine and lower plasma potassium, urinary pH, potassium, magnesium, phosphate and citrate than the controls. The patients had higher P-MDA, E-MDA, U-MDA, U-protein and NAG activity, but lower GSH, cGPx activity, protein thiol and vitamin E, when compared with controls. After potassium citrate supplementation, P-MDA and E-MDA decreased while plasma vitamin E, urinary NAG activity and citrate increased. Renal stone disease is associated with high oxidative stress and damage to renal tubular cells. These abnormalities are coincident with an increase in blood lipid peroxidation products and a decrease in antioxidant status. Although supplementation with potassium citrate improved urinary citrate levels and oxidative stress, it neither reduced urinary lipid peroxidation products nor remedied the damage to renal tubular cells, probably due to the existence of kidney stones.

Adult↗

PubMed2002

The optimal dose of potassium citrate in the treatment of children with distal renal tubular acidosis.

BACKGROUND: Distal renal tubular acidosis (RTA) is a common cause of intractable calcium nephrolithiasis. In adults, the use of potassium citrate (PC) in distal RTA effectively decreases metabolic acidosis and the risk of calcium oxalate stone but it cannot decrease the risk of calcium phosphate stone. However, there is no report for the optimal dose of PC and the risk of calcium stone in distal RTA in children. OBJECTIVE: To evaluate the optimal dose of PC that minimizes the risk of calcium nephrolithiasis in children with distal RTA. METHOD: Prospective study PATIENTS: Children who have distal RTA and were followed-up for 4 months. Patients were studied in a control phase, 1 month of PC 2 mEq/kg/day, 2 months of PC 3 mEq/kg/day and 1 month of PC 4 mEq/kg/day. The urine specimens of 41 normal children were measured for the reference value of the parameters determining the risk of calcium stone. RESULTS: Eight children (mean age of 10 +/- 3.7 years, female : male = 6: 2) with distal RTA were studied during the control phase and after receiving PC 2 mEq/kg/day for I month. Treatment with PC 2 mEq/kg/day was not able to normalize serum bicarbonate and caused no significant change in the urine citrate/creatinine ratio, and activity production of calcium phosphate stone but it caused a significant decrease in the urine calcium/citrate ratio. Although PC 3 mEq/kg/day for I month normalized plasma bicarbonate, only this dose given for 2 months caused a significant increase in the urine citrate/creatinine ratio and urine calcium/ citrate ratio to values that were not different from normal children, while the activity production of calcium phosphate stone did not decrease to normal level. The effect of PC 4 mEq/kg/day was similar to that of 3 mEq/kg/day. CONCLUSION: Potassium citrate 3 mEq/kg/day for 2 months effectively normalized serum bicarbonate and decreased the risk of calcium oxalate stone but this treatment was theoretically unable to reduce the risk of calcium phosphate stone in children with distal RTA.

Acidosis, Renal Tubular↗

PubMed1993

Inhibitory effect of potassium citrate on rat renal tumors induced by N-ethyl-N-hydroxyethylnitrosamine followed by potassium dibasic phosphate.

Potassium dibasic phosphate (PDP) was administered at a concentration of 10% by weight in basal diet to unilaterally nephrectomized Wistar rats previously given 1000 ppm N-ethyl-N-hydroxyethyl-nitrosamine (EHEN) in the diet for 2 weeks. To study the effect of alkalinization on renal mineralization, some animals concomitantly received 5% potassium citrate (PC). Feeding PDP alone promoted adenomatous hyperplasias, which were regarded as preneoplastic lesions, as well as renal cell tumors in EHEN-initiated rats, whereas the addition of PC to PDP diets reduced the promoting effect. Histopathology, serum biochemistry and urinalysis indicated retardation of renal calcium crystallization by PC. Two other phosphate salts, sodium phosphate (SP) and calcium phosphate (CP), were also administered. SP showed a slight promoting effect on adenomatous hyperplasias and a 2-fold increase in the yield of renal cell tumors, while CP induced a clear reduction of both lesions, over EHEN alone. The promoting effects of both PDP and SP and the inhibitory effect of PC were somewhat correlated to 5-bromo-2'-deoxyuridine labeling indices, the degree of nephropathy, and mineralization in the kidney. Immunohistochemically, the nephropathy induced by phosphate salts was not linked to alpha 2u-globulin. A pathogenesis for renal carcinogenesis is suggested in which nephropathy associated with mineralization enhances the development of renal cell tumors.

Alpha-Globulins↗

PubMed1999

Dietary potassium bicarbonate and potassium citrate have a greater inhibitory effect than does potassium chloride on magnesium absorption in wethers.

We addressed the question whether the type of anion in potassium salts affects magnesium absorption and the transmural potential difference by using wethers (n = 8) fed a control diet and diets supplemented with equimolar amounts of KHCO(3), KCl or K-citrate according to a Latin-square design. The control diet contained 10.9 g K/kg dry matter and the high K diets contained 41.3 g K/kg dry matter. Compared with the control diet, KHCO(3) and K-citrate significantly reduced apparent Mg absorption by 9.5 and 6.5%, respectively. Supplemental KCl tended to reduce (P = 0.070) group mean magnesium absorption by 5.5%. Consumption of supplemental KHCO(3) and K-citrate produced a significant increase in the transmural potential difference (serosal side = positive) by 17.1 and 20.7 mV, respectively, whereas the addition of KCl to the diet did not. The individual values for the four diets tended to show a negative correlation (r = -0.336, n = 32, P = 0.060) between the transmural potential difference and apparent magnesium absorption. We conclude that different potassium salts have different effects on magnesium absorption in ruminants as caused by different effects on the transmural potential difference.

Animals↗

PubMed1986

Successful management of uric acid nephrolithiasis with potassium citrate.

Eighteen patients with uric acid nephrolithiasis (six with uric acid stones alone and 12 with both uric acid and calcium stones) underwent long-term treatment (1 to 5.33 years, mean of 2.78 years) with potassium citrate (30 to 80 mEq/day, usually 60 mEq/day). Urinary pH increased from low (5.30 +/- 0.31 SD) to normal (6.19 to 6.46) during treatment. Urinary content of undissociated uric acid, which was high to begin with at 204 +/- 82 mg/day, decreased to the normal range (64 to 108 mg/day) following treatment. Urinary citrate rose from 503 +/- 225 mg/day to 852 to 998 mg/day. Urinary saturation of calcium oxalate significantly declined with potassium citrate treatment. New stone formation rate declined from 1.20 +/- 1.68 stones/year to 0.01 +/- 0.04 stones/year (P less than 0.001 by chi square). Remission was experienced in 94.4% of patients, and the group stone formation rate declined by 99.2%. Detailed case reports were obtained in five patients showing different responses between sodium alkali and potassium alkali treatment. All five patients had persistently low urinary pH (typically less than 5.5) and normouricosuria, and four had hyperuricemia. Before treatment, they had stones surgically removed or spontaneously passed, which were pure uric acid in composition. When sodium alkali was give (as bicarbonate or citrate, 60 to 118 mEq/day), new stone formation continued in four patients, and a radiolucent (uric acid) calculus become "calcified" in the remaining patient. The stone analysis disclosed calcium oxalate in five patients and calcium phosphate in three patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1994

Impact of sodium-potassium citrate on the diurnal variations in urinary calcium oxalate and calcium phosphate saturation levels in normal individuals.

OBJECTIVE: To study the effects of treatment for 5 days with sodium-potassium citrate (1 g three times a day (t.i.d.), 1 g four times a day (q.i.d.), or 3 g three times a day (t.i.d.)) on the diurnal variations of urinary calcium-containing lithogenic substances. SUBJECTS AND METHODS: Five healthy men participated in the study, in which the calcium oxalate (CaOx), octacalcium phosphate (OCP), hydroxyapatite (HAP), and brushite (Bru) urinary saturation levels in fractional urine samples were determined before and during treatment. RESULTS: The CaOx and Bru saturation levels, as estimated from the AP(CaOx) and AP(Bru) indices (Tiselius) respectively, peaked between 05.30 and 08.00 hours, and the peaks were blunted by each treatment regimen in comparison with the control day. In particular, the 1 g q.i.d. regimen significantly decreased the CaOx saturation level between 05.30 and 08.00 hours. The OCP and HAP saturation levels, as estimated from the AP(CaP) index (Tiselius), peaked between 08.00 and 10.30 hours, and the levels were increased by each regimen. In particular, the OCP level exceeded the formation product between 08.00 and 10.30 hours on day 5 in all regimens. CONCLUSION: An evening dose of sodium-potassium citrate in addition to the conventional t.i.d. regimen may reduce the early-morning urinary CaOx and Bru saturation levels whilst keeping OCP and HAP saturation within acceptable limits. In contrast, a morning dose may cause OCP saturation to exceed the formation product. Although the OCP saturation level during treatment was not significantly higher than the level before treatment, this slight increase might be critical.

Adult↗

PubMed1996

The lack of influence of long-term potassium citrate and calcium citrate treatment in total body aluminum burden in patients with functioning kidneys.

BACKGROUND: It has been suggested that citrate salts might enhance aluminum (Al) absorption from a normal diet, posing a threat of Al toxicity even in subjects with normal renal function. We have recently reported that in normal subjects and patients with moderate renal failure, short-term treatment with tricalcium dicitrate (Ca3Cit2) does not significantly change urinary and serum Al levels. However, we have not assessed total body Al stores in patients on long-term citrate treatment. OBJECTIVE: The objective of this study was to ascertain body content of Al non-invasively using the increment in serum and urinary Al following the intravenous administration of deferoxamine (DFO) in patients with kidney stones and osteoporotic women undergoing long-term treatment with potassium citrate (K3Cit) or Ca3Cit2, respectively. METHODS: Ten patients with calcium nephrolithiasis and five with osteoporosis who were maintained on potassium citrate (40 mEq/day or more) or calcium citrate 800 mg calcium/day (40 mEq citrate) for 2 to 8 years, respectively, and 16 normal volunteers without a history of regular aluminum-containing antacid use participated in the study. All participants completed the 8 days of study, during which they were maintained on their regular home diet. Urinary Al excretion was measured during a two-day baseline before (Days 5, 6) and for 1 day (Day 7) immediately following a single intravenous dose of DFO (40 mg/kg). Blood for Al was obtained before DFO administration, and at 2, 5 and 24 hours following the start of the infusion. RESULTS: The median 24-hour urinary Al excretion (microgram/day) at baseline versus post-DFO value was 15.9 vs. 44.4 in the normal subjects and 13.3 vs. 35.7 in the patients. These values were all within normal limits and did not change significantly following DFO infusion (p = 0.003 and p = 0.0001, respectively). The median change of 17.1 micrograms/day in urinary Al in the normal subjects was not significantly different from the 18.7 micrograms/day change measured in the patient group (p = 0.30). Similarly, no change in the mean serum Al was detected at any time following the DFO infusion, either in the patient or control group (patients 4.1 to 4.3 ng/ml, controls 7.4 to 4.6 ng/ml). CONCLUSION: The results suggest that abnormal total body retention of Al does not occur during long-term citrate treatment in patients with functioning kidneys.

Adult↗

PubMed1986

Successful treatment of hyperuricosuric calcium oxalate nephrolithiasis with potassium citrate.

Calcium stone (renal) formation in patients with hyperuricosuria has been ascribed to the urate-induced crystallization of calcium oxalate. Citrate (0.5mM), added to synthetic medium metastably supersaturated with respect to calcium oxalate, was shown to inhibit heterogeneous nucleation of calcium oxalate by monosodium urate (2 mg/mL). Long-term trial with potassium citrate (60 to 80 mEq/day) was therefore undertaken to determine whether induced hypercitraturia would prevent calcium oxalate stone formation in 19 patients with hyperuricosuria. The treatment produced a sustained rise in urinary pH by 0.55 to 0.85 to the high normal range (6.5 to 7.0). Urinary citrate levels rose by 249 to 402 mg/day to approximate the normal mean value of 643 mg/day. Commensurate with these changes, urinary saturation of calcium oxalate (relative saturation ratio) and the amount of undissociated uric acid declined significantly. However, the urinary uric acid and saturation of monosodium urate remained elevated. Stone formation declined from 1.55 +/- 2.70 per patient-year to 0.38 +/- 1.22 per patient-year during mean treatment period of 2.35 +/- 0.88 years. Stones ceased to form in 16 of 19 patients during treatment. The results provide physicochemical and clinical evidence for the utility of potassium citrate in the management of hyperuricosuric calcium oxalate nephrolithiasis.

Adult↗