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At least 19 recordsLinked to original sources
PubMed1987

[Diurnal variation in plasma oxalate concentration and oxalate clearance in calcium oxalate stone formers with special reference to the effect of oxalate loading].

The diurnal variations in the plasma oxalate concentration and oxalate clearance were examined at the state of oxalate restriction and loading on 6 normal subjects and 11 calcium oxalate stone formers. The oxalate-restricted diet contained 44.5 mg of total oxalate, 32.2 mg of soluble oxalate, and for oxalate loading, spinach (100 g: total oxalate 429 mg, soluble oxalate 156 mg) was added to the oxalate-restricted diet at breakfast. Normal subjects showed a diurnal variation in plasma oxalate at oxalate restriction and loading. The plasma oxalate concentration showed the highest level under the fasting condition, gradually dropped and was then fixed at the lower level during the day. The oxalate clearance during the day was significantly higher (p less than 0.05) than that during the night in normal subjects taking the oxalate restricted diet, and after they were oxalate loaded, it increased significantly (p less than 0.05) for 6 hours, but returned to the level at oxalate restriction during the night. Meanwhile, there was no significant difference in oxalate clearance between day and night in calcium oxalate stone formers. As compared with the control group, there were no significant differences in the diurnal variation in the plasma oxalate concentration, oxalate clearance at oxalate restriction, or in the diurnal variation of the plasma oxalate concentration at oxalate loading. However, the oxalate clearance during the night after oxalate loading increased significantly (p less than 0.05) compared with the control group. Based on the pattern of urinary oxalate excretion during the night compared with the control group, the stone formers were divided into two groups. The first group showed significantly (p less than 0.01) higher oxalate clearance during the night both during oxalate restriction and loading. The oxalate clearance increased significantly up to 8 hours after oxalate loading (p less than 0.01) and during the night (p less than 0.05) compared with the level during oxalate restriction. The plasma oxalate concentration did not increase after loading. The second group showed a significantly (p less than 0.05) lower oxalate clearance during the day after oxalate loading. The oxalate clearance (p less than 0.05) was significantly increased for 4 hours after the loading compared to the during oxalate restriction. The plasma oxalate concentration increased at 6 hours after oxalate loading. There was no significant difference in oxalate clearance during the night. The diurnal variation in plasma oxalate level, a decrease during the day and an increase during the night, was shown in both normal subjects and stone formers.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1979

Determination of oxalate in urine using oxalate oxidase: comparison with oxalate decarboxylase.

The oxalate content of urine is determined by means of oxalate oxidase and simple pH measurement. The enzyme specifically decarboxylates oxalate, producing two moles CO2 per mole oxalate. The CO2 diffuses into an alkaline buffer solution (Hallson, P. C. & Rose, G. A. (1974), Clin. Chim. Acta 55, 29--39) in the closed reaction vessel, and reduces the pH value, which is measured with an electrode. Only 125 microliter native urine is required to measure oxalate concentrations in the range of 80 mumol/l to 1.6 mmol/l (corresponding to 7 to 144 mg anhydrous oxalic acid per liter). The limit of detection is 10 nmol oxalate, and the accuracy is 101% with a coefficient of variation of 6%. The method described is insensitive to various interfering factors, such as reducing and oxidizing substances, cloudy or colored samples. It is therefore also suitable for oxalate determination in food technology and plant breeding.

Carboxy-Lyases↗
PubMed1987

Isolation from human calcium oxalate renal stones of nephrocalcin, a glycoprotein inhibitor of calcium oxalate crystal growth. Evidence that nephrocalcin from patients with calcium oxalate nephrolithiasis is deficient in gamma-carboxyglutamic acid.

We have determined that the organic matrix of calcium oxalate kidney stones contains a glycoprotein inhibitor of calcium oxalate crystal growth (nephrocalcin) that resembles nephrocalcin present in the urine of patients with calcium oxalate stones and differs from nephrocalcin from the urine of normal people. Pulverized calcium oxalate renal stones were extracted with 0.05 M EDTA, pH 8.0; nephrocalcin eluted in five peaks using DEAE-cellulose column chromatography, and each peak was further resolved by Sephacryl S-200 column chromatography. Four of the five DEAE peaks corresponded to those usually found in nephrocalcin from urine; the fifth eluted at a lower ionic strength than any found in urine. Amino acid compositions and surface properties of nephrocalcins isolated from kidney stones closely resembled those of nephrocalcins isolated from urine of stone-forming patients: they differed from normal in lacking gamma-carboxyglutamic acid residues, and in forming air-water interfacial films that were less stable than those formed by nephrocalcin from normal urine.

1-Carboxyglutamic Acid↗
PubMed1986

[Renal oxalate excretion following oral oxalate load in patients with urinary calculus disease and healthy controls].

Oral oxalate loading using sodium oxalate or a vegetable juice was done to evaluate the intestinal absorption of exogenous oxalate in 30 patients with renal stones and 13 healthy controls. Fifteen calcium oxalate stone formers, 7 non-oxalate stone formers and 10 healthy volunteers were given an oral loading of sodium oxalate (500 mg). Urinary oxalate increased promptly, reaching a peak value within 4 to 8 hours after administration of a synthetic oxalate orally in a fasting state. In calcium oxalate stone formers, the mean increment of urinary oxalate and the bioavailability following oral sodium oxalate load were significantly higher than in the healthy controls and non-oxalate stone formers. Furthermore, intestinal hyperabsorption of oxalate in our criterion was defined in six patients with calcium oxalate stones (40%). On the other hand, eight calcium oxalate stone formers and three healthy controls were given vegetable juice. Urinary oxalate was increased only slightly after the ingestion, and there was no difference between calcium oxalate stone formers and normal controls. These results suggest that a certain hyperoxaluria might be induced by intestinal absorption of exogenous oxalate, and that the hyperabsorption might indicate a possible risk factor for calcium oxalate stone formation.

Administration, Oral↗
PubMed1985

Spectrophotometric determination of oxalate in urine and plasma with oxalate oxidase.

In order to establish a standard procedure for the spectrophotometric determination of urinary and plasma oxalate with oxalate oxidase (Laker, M.F., et al. (1980) Clin. Chem. 26, 827-830; Sugiura, M., et al. (1980) Clin. Chim. Acta 105, 393-399) and to define the limitations of the method, the procedures and reactions involved in the assay have been examined. Among the chromogenic hydrogen donors for peroxidase tested, a combination of 3-methyl-2-benzothiazolinone hydrazone (MBTH) and sodium N-sulfopropylaniline (HALPS) was found to be best for the oxalate determination under the conditions used. Urine contained substance(s) which were inhibitory to the measurement of hydrogen peroxide by the peroxidase-catalyzed oxidative condensation of MBTH and HALPS, but they were largely removed by charcoal treatment at pH 5.6 without significant loss of oxalate. Deproteinization of plasma was carried out by ultrafiltration through a membrane cone (Centriflo CF-25) at neutral pH. The plasma oxalate ultrafiltrability under the conditions employed was calculated to be approximately 95%. A standard assay system for oxalate in these urine and plasma samples was then set up based on a series of studies on the reactions involved in the assay. In the case of normal plasma, however, the absorbance change was very small due to the low concentration of oxalate, and in addition, pretreatment of plasma with excess oxalate decarboxylase followed by the ultrafiltration and oxalate determination did not abolish completely the oxalate oxidase-dependent absorbance increase. It was concluded that the enzymic method was useful for the assay of urinary oxalate and in detecting elevated levels of plasma oxalate such as those in hemodialysis patients but was not sensitive enough to determine accurately the normal or decreased level of oxalate in plasma. The apparent concentration of oxalate in normal human plasma was measured in this work as 3.5 +/- 0.8 microM (mean +/- S.D., n = 8), and this result was interpreted to mean that the concentration of plasma oxalate was less than approximately 3.5 microM, as estimated by the present method.

Blood Proteins↗
PubMed1989

[Studies of oxalate efflux and oxalate transport via anion exchange in rat renal brush border membrane vesicles].

In order to study the characteristics of oxalate transport across the brush border membrane, we studied oxalate uptake and efflux by rat renal cortical brush border membrane vesicles (BBMV). The vesicles were prepared with MgCl2 precipitation method and oxalate uptake was measured by a modification of the rapid millipore filtration technique. In order to analyze efflux of oxalate from BBMV, the vesicles were pre-equilibrated with 100 microM [14-C]-oxalate for 10 min, at 30 degrees C. Temperature dependent and independent oxalate uptake were observed under the conditions of salt and anion free medium. Temperature dependent oxalate accumulation showed "over shoot", indicating carrier mediated oxalate flux. The stimulating effect of an inside alkaline pH gradient on oxalate uptake failed to show at intravesicular pH 8.5. The efflux of oxalate from pre-loaded BBMV showed three steps decreasing curve. Initial rapid efflux was inhibited by extravesicular 5 mM para-aminohippurate (PAH) and low temperature (5 degrees C). Extravesicular 100 microM PAH had no effect on oxalate efflux. These data suggested a carrier mediated oxalate transport system across the barrier from intracellular to luminal site. An outwardly directed chloride (Cl) gradient stimulated oxalate uptake in BBMV, DIDS, anion exchange inhibitor, inhibited this Cl-stimulated oxalate uptake completely. Harmaline, a Na-coupled cotransport inhibitor, had no effect and Probenecid, an organic anion transport inhibitor, caused 45% inhibitory effect on Cl-gradient stimulated oxalate transport system via anion exchange in the rat kidney BBMV.

Animals↗
PubMed1991

Plasma oxalate levels rise in hemodialysis patients despite increased oxalate removal.

The cause of secondary hyperoxalemia and oxalosis in patients on maintenance dialysis is unknown. The oxalate removal rate was determined in 26 patients on maintenance hemodialysis and 6 on continuous ambulatory peritoneal dialysis by measuring oxalate removed by dialysis and urinary excretion. The role of vitamin B6 deficiency and ascorbate in the raised plasma oxalate concentrations of these patients was evaluated. Plasma oxalate in hemodialysis patients, 442 +/- 41 micrograms/100 mL (mean +/- SE), and peritoneal patients, 394 +/- 115 micrograms/100 mL, were significantly higher than that in normal subjects, 11 +/- 1 microgram/100 mL (P less than 0.001). Average daily oxalate removal in subjects on hemodialysis, based on dialysis losses and urinary excretion, 35 +/- 3 mg/24 h, was significantly greater than urinary excretion of normal subjects, 26 +/- 1 (P less than 0.01). Oxalate removal from peritoneal dialysis patients, 28 +/- 2 mg/24 h, was not significantly different from that of hemodialysis patients or urinary excretion of normal subjects. Plasma ascorbate and B6 status were not correlated with plasma oxalate. A positive correlation between B6 deficiency and oxalate removal rate was not found. Plasma oxalate was correlated with time on dialysis (all patients) (P = 0.02). In a separate study of 15 hemodialysis patients followed over 2.3 +/- 0.2 yr, both plasma oxalate and oxalate removal rate significantly increased, P less than 0.001 and 0.05, respectively. It was concluded that oxalate removal rate is increased in hemodialysis patients and that the increased total body oxalate burden in these patients is not due to decreased removal. Although the increase may result from increased oxalate synthesis or gastrointestinal absorption, B6 deficiency and increased plasma ascorbate do not play a role.

Alanine Transaminase↗
PubMed1986

Evidence that serum calcium oxalate supersaturation is a consequence of oxalate retention in patients with chronic renal failure.

Serum oxalate rises in uremia because of decreased renal clearance, and crystals of calcium oxalate occur in the tissues of uremic patients. Crystal formation suggests that either uremic serum is supersaturated with calcium oxalate, or local oxalate production or accumulation causes regional supersaturation. To test the first alternative, we ultrafiltered uremic serum and measured supersaturation with two different methods previously used to study supersaturation in urine. First, the relative saturation ratio (RSR), the ratio of the dissolved calcium oxalate complex to the thermodynamic calcium oxalate solubility product, was estimated for 11 uremic (before and after dialysis) and 4 normal serum samples using a computer program. Mean ultrafiltrate oxalate predialysis was 89 +/- 8 microM/liter (+/- SEM), 31 +/- 4 postdialysis, and 10 +/- 3 in normals. Mean RSR was 1.7 +/- 0.1 (predialysis), 0.7 +/- 0.1 (postdialysis), and 0.2 +/- 0.1 (normal), where values greater than 1 denote supersaturation, less than 1, undersaturation. Second, the concentration product ratio (CPR), the ratio of the measured calcium oxalate concentration product before to that after incubation of the sample with calcium oxalate monohydrate crystal, was measured in seven uremic and seven normal serum ultrafiltrates. Mean oxalate was 91 +/- 11 (uremic) and 8 +/- 3 (normal). Mean CPR was 1.4 +/- 0.2 (uremic) and 0.2 +/- 0.1 (normal). Predialysis, 17 of 18 uremic ultrafiltrates were supersaturated with respect to calcium oxalate. The degree of supersaturation was correlated with ultrafiltrate oxalate (RSR, r = 0.99, r = 29, P less than 0.001; CPR, r = 0.75, n = 11, P less than 0.001). A value of ultrafiltrate oxalate of 50 microM/liter separated undersaturated from supersaturated samples and occurred at a creatinine of approximately 9.0 mg/dl.

Adult↗
PubMed1989

Bioavailability of oxalic acid from spinach, sugar beet fibre and a solution of sodium oxalate consumed by female volunteers.

Oxalate bioavailability from sugar beet fibre (40 g), spinach (25 g) and a solution of sodium oxalate (182 mg) was tested in nine women using a triplicated 3 x 3 Latin square arrangement. Each test substance provided 120 mg oxalic acid. Throughout the study the volunteers consumed a control diet and the test substances were administered at breakfast on specified days. After an initial 2-day control period, oxalate was administered in three test periods that consisted of one test day followed by one control day. Urine collected during 24-hr periods was analysed daily for oxalate. Oxalate excretion did not differ among the five control days and was not increased significantly following the ingestion of sugar beet fibre by the volunteers. Oxalate excretion was greater (P less than 0.0001) for the mean of the spinach and sodium oxalate solution diets than for the mean of the sugar beet fibre and control diets. Oxalate bioavailability from sugar beet fibre was 0.7% compared with bioavailabilities of 4.5 and 6.2% for spinach and oxalate solutions, respectively. The low bioavailability of oxalate from sugar beet fibre may be attributable to its high ratio of minerals (calcium and magnesium) to oxalate, its complex fibre matrix or the loss of the soluble oxalate during processing of sugar beets.

Administration, Oral↗
PubMed1985

Plasma oxalate concentration and oxalate distribution volume in patients with normal and decreased renal function.

In twenty-one patients (sixteen male, five female) with various kidney diseases including primary hyperoxaluria type I (four patients), the plasma oxalate level was calculated from the isotopically determined oxalate clearance and the chemically determined urinary oxalate excretion. The apparent oxalate distribution volume was assessed as well. In patients with impaired kidney function (n = 12), the oxalate clearance was lower and the biological half-life and plasma concentration were higher than in patients with normal kidney function (n = 10). No differences were found in the oxalate-to-creatinine clearance ratio (mean value 1.93), urinary oxalate excretion and apparent oxalate distribution volume. A linear relation was found between the oxalate and creatinine clearance, while the clearance ratio was independent of the degree of renal failure. The apparent oxalate distribution volume was 1.45 times the estimated extracellular fluid volume. Because the isotopically determined plasma oxalate levels are lower than chemically measured ones, a quick and better estimation of plasma oxalate can be made from the urinary oxalate excretion and the creatinine clearance.

Adolescent↗
PubMed1978

Renal oxalate excretion following oral oxalate loads in patients with ileal disease and with renal and absorptive hypercalciurias. Effect of calcium and magnesium.

Intestinal absorption of oxalate was assessed indirectly from the increase in renal oxalate excretion following the oral administration of 5 mmol of stable oxalate. When sodium oxalate alone was given without divalent cations to patients in the fasting state, the urinary oxalate increased promptly (within 2 hours). The increase was more prominent and sustained in those with ileal disease (ileal resection or jujunoileal bypass); thus, 35 per cent of the orally administered oxalate eventually appeared in the urine in the group with ileal disease, 8 per cent in the group with stones (renal and absorptive hypercalciurias) and 9 per cent in the control group. This hyperexcretion of oxalate could be largely, but not totally, ameliorated by the concurrent oral administration of divalent cations. Although urinary oxalate decreased significantly following the oral administration of calcium or magnesium, hyperoxaluria persisted in most patients. The results suggested that the hyperabsorption of oxalate in ileal disease cannot be accounted for solely by an increased absorbable oxalate pool associated with calcium-fatty acid complexation. Moreover, although urinary oxalate decreased, urinary calcium increased concurrently when either calcium or magnesium was given. Thus, there was no significant change or increase in the urinary state of saturation with respect to calcium oxalate.

Administration, Oral↗
PubMed1985

Estimation by infrared spectrophotometer of the calcium oxalate dihydrate to calcium oxalate monohydrate ratio.

According to the theoretical expression for calibration curve as a function of the optical absorption ratio of two peaks and with the analysis of the infrared spectra of the mixture samples of commercial calcium oxalate monohydrate and synthesized calcium oxalate dihydrate, the following quadratic equation was obtained; Y = 1.79 X2 - 30.90 X + 107.04 in which Y is the percentage of the purity of calcium oxalate dihydrate and X is the ratio of the relative optical absorption at 660 cm.-1 (the wave number at a characteristic absorption peak of calcium oxalate monohydrate) to that at 610 cm.-1 (that of calcium oxalate dihydrate) by regarding the line as a base-line that links the absorption valley at around 700 cm.-1 with that at 550 cm.-1 The linear correlation coefficient of the actual purity to the estimated purity obtained from this formula of calcium oxalate dihydrate is 0.995. When this formula is applied to the results derived from the infrared spectra of the mixture samples of commercial calcium oxalate monohydrate and calcium oxalate dihydrate obtained from urinary stones in duplicate in each percentage, the linear correlation coefficient is 0.991. This estimation method by infrared spectrophotometer of the calcium oxalate dihydrate to calcium oxalate monohydrate ratio gave a very close correlation between actual and estimated purity of calcium oxalate dihydrate and seems useful in the study of calcium oxalate urolithiasis.

Calcium Oxalate↗
PubMed1991

Correction of erythrocyte abnormalities in idiopathic calcium-oxalate nephrolithiasis and reduction of urinary oxalate by oral glycosaminoglycans.

Calcium-oxalate nephrolithiasis is associated with a defect in erythrocyte oxalate self-exchange and an abnormal rate of erythrocyte membrane protein phosphorylation. There is evidence that glycosaminoglycans (GAGs) have a regulatory effect on both of these processes. This study tested the hypothesis that modifications of erythrocyte oxalate self-exchange induced by oral GAGs are paralleled by similar changes in overall oxalate metabolism. 40 patients with idiopathic calcium-oxalate nephrolithiasis were treated for 15 days with 60 mg/day of a mixture of GAGs. By day 15 of treatment there were significant reductions from baseline in erythrocyte oxalate self-exchange (mean [SD] 1.67 [1.18] vs 2.59 [1.63] x 10(2) per min; p less than 0.005) and erythrocyte membrane protein phosphorylation (55.8 [7.3] vs 72.9 [6.8] x 10(-3) cpm/mg protein; p less than 0.005), but also in urinary oxalate excretion (0.24 [0.09] vs 0.31 [0.15] mmol/24 h; p less than 0.005). This finding suggests similar changes in both erythrocytes and other cells more important in oxalate handling. The changes had reversed by 15 days after withdrawal of treatment. Acute intravenous administration of GAGs (60 mg) induced a fall in carbon-14-labelled oxalate renal clearance (143 [13] vs 169 [28] ml/min; p less than 0.005), which strongly suggests the participation of the kidney. However, reduced oxalate absorption from the intestine, and even decreased synthesis of oxalate, cannot be ruled out.

Administration, Oral↗
PubMed1988

Intestinal oxalate-degrading bacteria reduce oxalate absorption and toxicity in guinea pigs.

Previous studies have provided evidence that an anaerobic bacterium, which degrades dietary oxalate to CO2 and formate, is present in colonic contents of a number of herbivorous species, laboratory rodents and humans. The present study examines the possibility that these bacteria degrade significant amounts of oxalate and can influence colonic oxalate absorption. Guinea pigs adapted to a diet containing 2% sodium oxalate or fed a normal diet were challenged with 67, 135, 170 or 200 mg of sodium oxalate containing 0.5 microCi of [14C]oxalate, which was injected into the cecum. Adapted animals excreted approximately 2% of the 14C in the urine, regardless of the dose, whereas unadapted animals excreted significantly higher amounts in the urine at the two lower doses and died at the two higher doses. Conversely, antibiotic treatment of adapted guinea pigs reduced the ability of their cecal flora to degrade oxalate, and a correspondingly greater percentage of an injected oxalate load was excreted in the urine. Oxalate degradation rates in cecal fluid were depressed by the secondary bile salt deoxycholate, and in vitro studies with pure isolates of guinea pig and human strains of oxalate degraders confirmed that these bacteria were highly sensitive to low concentrations of deoxycholate. Results indicate that these bacteria may be important in preventing excess absorption of oxalate and raise the possibility that the hyperoxaluria associated with bile salt malabsorption of ileal disease in part may be due to suppression of these bacteria by the bile salts.

Adaptation, Physiological↗
PubMedDate not supplied

Urinary oxalate recovery after oral oxalic load: an alternative method to the quantitative determination of stool fat for the diagnosis of lipid malabsorption.

Urinary oxalate concentrations were measured in 45 patients with quiescent Crohn's disease, four patients with chronic pancreatitis and five healthy subjects after a normal oxalate (150 g/day) diet, after a high-fat (150 g/day), normal oxalate diet and after and after a high-oxalate (500 mg/day) diet. Urinary oxalate concentrations were significantly (P less than 0.05) higher in patients with Crohn's disease and steatorrhoea, but not in those with chronic pancreatitis, after administrating a high-oxalate diet compared with healthy subjects. Mean oxalate values were 19.1 mg/24 h in controls compared with 65.8 mg/24 h in Crohn's disease patients. A direct correlation (r = 0.37, P less than 0.01) was established between faecal rats and urinary oxalate after oval oxalate load: this correlation (r = 0.43, P less than 0.01) is closer when only patients with Crohn's disease are considered. The study, therefore, confirmed a correlation between steatorrhoea and hyperoxaluria in patients with Crohn's disease; however, the high percentage of false positive results limits the use of urinary oxalate concentrations as a reliable indicator of lipid malabsorption. It is concluded that, at present, measurement of urinary oxalate cannot be recommended as a valid alternative to the Van de Kamer method for diagnosing lipid malabsorption.

Adolescent↗
PubMed1991

[Oxalate as a promoter in calcium oxalate nephrolithiasis].

Oxalate transports on membranes of red blood cell, intestinal epithelium and proximal tubule cell were reviewed, and the new findings about oxalate transport across these membranes are reported. Red blood cell oxalate influx rate in a group of recurrent calcium oxalate stone formers was significantly higher than that of a control group. In the red blood cells of mammals, the band 3 protein transports oxalate. Although abnormal influx rate of red blood cells might be recognized as an expression of somatic cell abnormality of oxalate transport in some recurrent stone formers, the band 3 protein is not related to oxalate transport in both kidney and intestine. The study using brush border membrane vesicles suggested the presence of Na-oxalate co-transport. In humans, sodium intake increased the oxalate/creatinine ratio of urine. This indicated that excessive sodium intake might be a risk factor of stone formation. Further study of oxalate transport of both kidney and intestine will be required to elucidate an etiology of calcium oxalate nephrolithiasis.

Animals↗
PubMed1990

Glycosaminoglycan content, oxalate self-exchange and protein phosphorylation in erythrocytes of patients with 'idiopathic' calcium oxalate nephrolithiasis.

1. This study was performed to test the hypothesis that glycosaminoglycans may play an important role in the observed abnormalities in oxalate flux seen in patients with calcium oxalate nephrolithiasis. 2. Oxalate flux rate, erythrocyte membrane glycosaminoglycan content, membrane protein phosphorylation and effect of heparan sulphate on erythrocyte oxalate flux in vitro were studied in control subjects and patients with calcium oxalate nephrolithiasis. 3. In comparison with control subjects, renal stone-formers showed a significantly higher oxalate self-exchange, a lower erythrocyte membrane glycosaminoglycan content and a higher membrane phosphorylation rate. In stone-formers, erythrocyte glycosaminoglycan content correlated inversely with both oxalate flux rate and protein phosphorylation. In vitro, heparan sulphate promoted a significant fall in the rate of oxalate self-exchange. 4. These findings support the hypothesis that a lower erythrocyte membrane content of glycosaminoglycans enhances membrane protein phosphorylation, leading to an increased rate of transmembrane oxalate flux.

Adult↗