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At least 1,063 records · Page 59Linked to original sources
PubMed1979

Oxalic acid concentration in serum measured by isotopic clearance technique. Experience in hyper- and normo-oxaluric subjects.

In a family from which two children suffered from primary hyperoxaluria the renal clearance of (14C) oxalate was studied. The (14C) oxalate/creatinine clearance ratio ranged from 1.76-2.63 (mean: 2.03) and appeared to be independent of glomerular filtration rate (GFR). The calculated plasma oxalate concentrations in normo-oxaluric subjects ranged from 0.1-0.9 mumol/L, whereas in hyperoxaluric subjects values between 3.2-16.3 mumol/L were found. The mean biological half-life of (14C) oxalate was 2.7hr in subjects with normal renal function and increased proportionally with renal functional impairment. Recovery of (14C) oxalate ranged from 87-112% (mean: 101%). All urine (14C) activity was found in the oxalate fraction.

Adolescent↗
PubMed1983

Ion-chromatographic measurement of oxalate in unprocessed urine.

We describe a sensitive, simple technique for determining urinary oxalate. Urine, diluted as necessary with distilled water, is injected into an ion chromatograph. Oxalate is detected conductimetrically as a distinct peak near the tail of the chromatogram. This peak specifically represents oxalate, because it is abolished if the sample is treated with oxalate decarboxylase. We have used this technique to measure oxalate in more than 3000 consecutively received urine samples. It has a CV of 6%.

Carbonic Acid↗
PubMed1984

Oxalate content in common Japanese foods.

The radioenzymatic method was used to determine the oxalate contents in common Japanese foods. High concentrations of oxalate were detected in spinach, Perilla frutescens, pepper, sesame, chocolate, and tea. Beer and coffee also contained some oxalate. Fruit and meat were low in oxalate content. Therefore, among the common Japanese foods, the most important foods to be avoided to restrict oxalate intake are chocolate, tea, and spinach.

Cacao↗
PubMed1978

Kinetics of early time calcium oxalate nephrolithiasis.

This paper examines the kinetics of calcium deposition in rat kidneys after an intraperitoneal sodium oxalate injection. From the results we conclude that only a limited portion of tubular surface is available for adsorption of calcium oxalate crystals, that adsorpption of calcium oxalate crystals onto tubular epithelium is a process of greater than first order with regard to the dose, and that the washout of retained particles from the tubules is a first-order process as related to time. Also, we conclude that in these animals, which were subjected to a large oxalate challenge, the deposition of calcium oxalate crystals is virtually all intratubular.

Animals↗
PubMed1984

Enzymic assay for oxalate in unprocessed urine, as adapted for a centrifugal analyzer.

In this automated modification of the oxalate decarboxylase method, oxalate can be measured (12 per hour) in acidified but otherwise unprocessed urine. Standard curves are linear up to at least 2.5 mmol/L. When 0.50 mmol of oxalate was added per liter to samples of 18 patients' urines, a mean analytical recovery of 98.5% (SD 3.6%) was obtained. Within-series CVs were 3.4 and 1.0%, between-series CVs 7.3 and 2.7% (n = 15) for oxalate concentrations of 0.31 and 0.61 mmol/L. The lower limit of detection is 25 mumol/L. Concentrations measured with this "direct" method correlated well (r = 0.95) with those measured after precipitation with calcium and ethanol and resolubilization in dilute sulfuric acid. For 17 healthy volunteers the mean urinary excretion of oxalate was 0.37 (SD 0.14) mmol/24 h.

Carboxy-Lyases↗
PubMed1982

Simple, reliable chromatographic measurement of oxalate in urine.

In this assay for oxalate in urine, oxalate is adsorbed from the urine onto graphitized carbon black (Carbopack B). After desorption and removal of the solvent, oxalic acid is gas-chromatographically measured after being derivatized with BF3/methanol. Chromatography is on Carbopack B/polyethylene glycol (Mr 20000), 93.7/6.3 by weight. The lower limit of detection of urinary oxalate is about 3 mg/L (CV less than or equal to 3.6%). A series of oxalate determinations in 24-h urine samples of 15 subjects gave a mean of 47.1 (SD 15.4) mg/24 h, with an analytical recovery of 97.4% (SD 3.0%, range 93.6-102.4%). Total analysis time for one sample is about 2 h.

Chromatography, Gas↗
PubMed1980

Excretion of urinary calcium and oxalate on three diets in patients with urolithiasis.

Effects of standard mineral, free, and low calcium--low oxalate diets on the urinary excretion of calcium and oxalate were studied in 153 consecutive patients with single or recurrent renal/ureteral stone. The patients were divided into four groups: 78 men with single stone (MS), 40 men with recurrent stone (MR), 30 women with single stone (WS), and 5 women with recurrent stone (WR). The urine volume was altered significantly (p less than 0.001) by the diet. The sex and the diet had a significant influence on the urinary excretion of calcium. The urinary excretion of oxalate was altered significantly by the diet (p less than 0.001), but not by sex nor by the number of stones. The goal for the low calcium--low oxalate diet (the simple concentration product under 26) was reached in MS and WS. The excretion of urinary calcium and oxalate increased and urine volume decreased in the samples collected at home when compared with the samples collected in the hospital. This was interpreted as a failure of the dietary regimen at home.

Adolescent↗
PubMed1981

Nucleation kinetics in the calcium oxalate-sodium urate monohydrate system.

The nucleation kinetics of calcium oxalate were studied in the presence and absence of sodium urate monohydrate crystalline material by three experimental measurements. These included analytical determinations of calcium and radiotracer analysis of oxalate in the metastable calcium oxalate solution phase and the independent detection of new crystal nuclei by solution turbidity measurements. None of the methods gave any evidence that sodium urate increases the induction time for nucleation of calcium oxalate, in contrast to previously published reports. These results are discussed in relation to the mechanisms advanced to explain the interdependency of hyperuricosuria and calcium oxalate urolithiasis.

Allopurinol↗
PubMed1994

Effect of urinary macromolecules and chondroitin sulphate on calcium oxalate crystallization in urine.

After filtration and ultrafiltration (10 kD) of 24 hour urine specimens from 12 healthy male subjects, calcium oxalate crystallization was induced in the filtered (FILTD) and ultrafiltered (UF) fractions by administration of a sodium oxalate load. In addition crystallization was also induced in UF fractions to which physiological quantities of chondroitin sulphate (CHON) had been added (UF+CHON). The rate of calcium oxalate crystallization was determined by measuring the rate at which turbidity increased. Crystal numbers and sizes were measured with a Malvern particle size analyzer and by scanning electron microscopy. Crystallization rates, crystal numbers and crystal sizes were generally lower in UF fractions than in FILTD fractions suggesting that urinary macromolecules are promoters of calcium oxalate crystallization. No increase in crystallization rate, crystal numbers or sizes occurred when chondroitin sulphate was added to UF fractions, indicating that the promoter activity of urinary macromolecules is not due to this particular glycosaminoglycan. On the contrary, crystallization rates were qualitatively lower in UF+CHON fractions than in UF fractions alone, suggesting a possible inhibitory role for chondroitin sulphate in real urine. Scanning electron microscopy revealed that while aggregates were present in UF and FILTD fractions, they were absent in UF+CHON fractions. This observation indicates that chondroitin sulphate might be an inhibitor of calcium oxalate crystal aggregation in real urine.

Adult↗
PubMed1994

Effect of uric acid on sodium oxalate-induced urolithiasis in rats--biochemical and histological evidences.

Effect of uric acid on sodium oxalate-induced biochemical and histological changes were studied in rats. Rats injected with sodium oxalate (0.7 mg/100 g body wt, ip) show calcium deposits in the lumen of kidney tubules. Uric acid administration was found to potentiate calcium oxalate calculi formation. Lipid peroxide formation was increased up to 100% in kidney and 28% in liver by sodium, oxalate treatment. Uric acid administration was found to reduce lipid peroxide level up to 12% in liver and 20% in kidney. From this study it is concluded that lipid peroxidation may not be the cause of sodium oxalate-induced urolithiasis and the results are discussed with reference to the epitaxic nature of uric acid on kidney stone formation.

Animals↗
PubMed1976

[Calcium metabolism in lactating goats: influence of sodium oxalate, sodium citrate and EDTA].

The influence of 2 p. 100 sodium oxalate, 4,57 p. 100 sodium citrate and 0,4 p. 100 Na2EDTA on various aspects of calcium metabolism and on milk characteristics has been studied in lactating goats. Sodium oxalate leads to no modifications of the variables studied : digestibility coefficient, biological valu+, coefficient of nutritive utilization and the coefficient of body retention. The only appreciable effect of sodium oxalate was on the amount of absorbed and utilized calcium which is diverted towards milk. These two values are decreased in the presence of oxalate. When sodium oxalate and sodium citrate were simultaneously added to the diet, citrate was shown to have no effect on digestibility, biological value, the coefficient of nutritive utilization and the coefficient of body retention, but did, however, considerably increase the amount of utilized calciun which was diverted towards milk. Concerning Na2EDTA, despite its higher calcium mobilizing power, it had no effect on the digestibility coefficient, the biological value, the coefficient of nutritive utilization and the coefficient of body retention; neither did it have an effect on the level of incorporation of calcium into milk. Calcium digestibility was cleorly higher in the latter two groups, where calcium ingestion was lower and milk production higher, conditions which both favorize calcium absorption.

Animals↗
PubMed1995

Experimental calcium oxalate nephrolithiasis and the formation of human urinary stones.

Calcium oxalate nephrolithiasis in rats requires induction of hyperoxaluria which results in increased urinary calcium oxalate supersaturation. As a result of low to mild chronic hyperoxaluria, calcium oxalate crystals deposit first in the papillary collecting ducts. Crystal deposition in the kidneys is preceded by calcium oxalate crystalluria and starts with the retention of aggregated calcium oxalate crystals in the renal tubules. Retained crystals move from the tubules to the interstitium, and in the process, become anchored to the tubular basement membrane. Crystal aggregates present in the superficial peripheral collecting ducts of the renal papillae ulcerate through to the papillary surface and grow into the stones.

Animals↗
PubMed1995

Oxalate-induced damage to renal tubular cells.

Our own studies and those of others have shown that the incidence of calcium oxalate stones and plaques is markedly increased by nephrotoxins. The possible role of oxalate as a nephrotoxin has not been fully appreciated. However, recent studies in experimental animals and in cultured cells support this possibility. The results of these studies led us to hypothesize that hyperoxaluria promotes stone formation in several ways: by providing a substrate for the formation of the most common form of renal stones, calcium oxalate stones, and by inducing damage to renal epithelial cells. Damaged cells in turn would produce an environment favorable for crystal retention and provide membranous debris that promotes crystal nucleation, aggregation and adherence. The present report summarizes evidence for oxalate nephrotoxicity and discusses the potential importance of oxalate toxicity in the pathogenesis of stone disease.

Animals↗
PubMed1997

[Inhibitory effect of oral administration of Takusya on calcium oxalate crystallization in human whole urine].

We previously reported that Takusya had the inhibitory effect on in vitro calcium oxalate crystallization and in vivo stone formation in an animal model and it could be a prophylactic agent against calcium oxalate stone formation. We studied the effect of Takusya on calcium oxalate crystallization in human urine. Takusya (500 mg/day and 1,000 mg/day) was administered to 16 healthy men for 3 days and then 24-hour urine samples were collected to measure the urinary excretion of calcium, phosphate, magnesium, uric acid, creatinine, citric acid and oxalic acid. The urine samples before the administration of Takusya was used as a control. The size and distribution of crystals, which were formed in the urine samples by adding calcium chloride and sodium oxalate, were measured using the Coulter counter technique. Urinary magnesium excretion was significantly reduced by 1,000 mg/day of Takusya compared with the control (p < 0.05). The growth of crystals was significantly inhibited by 500 mg/day of Takusya in the large crystal formers whose urine created crystals more than 3.5 microns before the administration of Takusya (p < 0.05). These findings suggested that Takusya inhibited the growth of crystals formed in human urine.

Administration, Oral↗
PubMed1998

[Effect of chorei-to and gorei-san on calcium oxalate crystallization in human urine].

The inhibitory effect of two kinds of Kampou medicine, Chorei-to and Gorei-san, on calcium oxalate crystallization in human urine, was examined. Chorei-to or Gorei-san was administered to 15 healthy male volunteers for three consecutive days under normal dietary conditions and 24-hour urine samples were collected before and after the administration. Urinary parameters including calcium, phosphorus, uric acid, oxalate and citrate were measured on each sample obtained. The inhibitory effect on calcium oxalate crystallization was examined using part of the collected 24-hour urine. There was no significant difference in urinary parameters before and after Chorei-to administration. Gorei-san administration significantly increased magnesium excretion in urine. A significant inhibitory effect on calcium oxalate crystallization in human urine was recognized when Gorei-san was administered, whereas Chorei-to had no inhibitory effect on calcium oxalate crystallization in urine.

Adult↗
PubMed1996

Calcium oxalate crystallization in urine of healthy men and women: a comparative study.

This study aimed to compare calcium oxalate (CaOx) crystallization in undiluted urine from healthy men and women with the object of clarifying the difference in stone incidence between the two sexes. Twenty-four hour urine specimens were collected from 37 men and 28 women. Urinary pH, and concentrations of Ca, oxalate and urate were measured, and indices of crystallization determined by Coulter Counter particle analysis following induction of CaOx crystallization by addition of oxalate. The amount of oxalate required to induce crystallization was significantly (p < 0.01) higher in females than in males, as was the overall particle volume deposited after 90 minutes incubation (p < 0.006). Scanning electron microscopy revealed larger individual crystals in female urine, and a greater degree of crystal aggregation in male urine, although the average overall size of the precipitated crystal particles did not differ between the two sexes. There were no significant differences between men and women with regard to median pH, or Ca and oxalate concentrations, but the median urate concentrations were slightly, but significantly, higher (p < 0.05) in the women's urines than in the men's. It was concluded that the greater risk of CaOx stones in men is related to an increased propensity to nucleate CaOx crystals per se, rather than to a tendency to form larger crystalline particles.

Adolescent↗
PubMed1986

Inhibition of calcium oxalate monohydrate (COM) crystal growth by pyrophosphate, citrate and rat urine.

An assay system for the measurement of the rate of Calcium Oxalate Monohydrate (COM) seed crystal growth in a metastable solution of calcium chloride and sodium oxalate containing traces of 14C-oxalic acid was used to assess the inhibitory activity of pyrophosphate (10(-5) M-10(-4) M), citrate (10(-4) M-10(-3) M) and urines of normal and pyridoxine deficient rats. Both pyrophosphate and citrate were strong inhibitors of COM crystal growth and caused a 50% decrease in crystal growth rate at 1.50 X 10(-5) M and 2.85 X 10(-4) M respectively. Normal rat urine strongly inhibited the COM crystal growth, while pyridoxine deficient animals showed a significant (p less than 0.01) decrease in mean inhibitory activity as compared to pair-fed controls. A lowered urinary inhibitory potential accompanied with hyperoxaluria and hypercalciuria, which is known to be associated with pyridoxine deficiency, may be a contributory risk of calcium oxalate crystallization and stone formation.

Animals↗
PubMed1991

Simple tests to determine urinary risk factors and calcium oxalate crystallization in the outpatient clinic.

We developed 2 simple and rapid tests for measurement of constituent concentrations and the stone-forming tendency of urine in the outpatient clinic. The concentrations of urinary constituents of calcium, magnesium, phosphorus, uric acid and oxalic acid were measured using 2 types of simple colorimetric tests (vial and quantitative filter types). The intensity of the color developing after a given interval was compared with a color standard of 4 levels. The results obtained using the colorimetric test were slightly lower in value than but significantly correlated with those obtained with standard measurements. The second test measured the crystal-forming ability of urine. A 10 ml. urine sample was pipetted into 4 vials that each contained different concentrations of oxalic acid and calcium. After a given interval the turbidity in each vial was compared with a control (0 mg. oxalic acid and calcium). If turbidity occurred in urine with low concentrations of oxalic acid and calcium the sample had a large tendency for crystals to form.

Ambulatory Care↗