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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↗
PubMed1993

Effect of dietary oxalate and calcium on urinary oxalate and risk of formation of calcium oxalate kidney stones.

Dietary restriction of oxalate intake has been used as therapy to reduce the risk of recurrence of calcium oxalate kidney stones. Although urinary oxalate is derived predominantly from endogenous synthesis, it may also be affected by dietary intake of oxalate and calcium. The risk of increasing urinary oxalate excretion by excessive consumption of dietary oxalate is greatest in individuals with a high rate of oxalate absorption, both with and without overt intestinal disease. Although oxalate-rich foods enhanced excretion of urinary oxalate in normal volunteers, the increase was not proportional to the oxalate content of the food. Only eight foods--spinach, rhubarb, beets, nuts, chocolate, tea, wheat bran, and strawberries--caused a significant increase in urinary oxalate excretion. Restriction of dietary calcium enhances oxalate absorption and excretion, whereas an increase in calcium intake may reduce urinary oxalate excretion by binding more oxalate in the gut. This review of the literature indicates that initial dietary therapy for stone-forming individuals can be limited to the restriction of foods definitely shown to increase urinary oxalate. The effects of oxalate-restricted diets on urinary oxalate should be evaluated by means of laboratory analyses of urine composition. Subsequent long-term therapy can be recommended if beneficial results are obtained from oxalate restriction at an appropriate calcium intake.

Animals↗
PubMed1999

Intestinal hyperabsorption of oxalate in calcium oxalate stone formers: application of a new test with [13C2]oxalate.

In up to one-third of patients with calcium oxalate stones, a hyperoxaluria can be detected. Hyperoxaluria can result from increased endogenous production, from excessive oxalate content of the food, or from intestinal hyperabsorption. For a causal therapy, it is important to discriminate between metabolic and hyperabsorptive hyperoxaluria. Our new 13C-oxalate test allows this differentiation. Under standardized conditions, 50 mg of disodium salt of [13C2]oxalic acid was applied. From the amount of labeled oxalate excreted in urine as measured by a gas chromatographic-mass spectrometric assay, the intestinal absorption was calculated. Seventy patients with recurrent calcium oxalate urolithiasis who had no signs of inflammatory bowel disease were tested. Their mean intestinal oxalate absorption was 9.2+/-5.1%. This was significantly higher than the mean absorption of 50 healthy volunteers (6.7+/-3.9%). There was no difference in oxalate absorption between male (n = 25) and female volunteers. Oxalate absorption correlated with the oxalate excretion in the 24-h urine (volunteers: r = 0.46, P < 0.01; patients: r = 0.62, P < 0.001). Oxalate hyperabsorption was defined as an absorption exceeding 10%. According to this definition, 34% of the patients had oxalate hyperabsorption; 20% of the volunteers showed a hyperabsorption, too. The 13C-oxalate absorption test allows reliable determination of intestinal oxalate absorption. Because of the use of a stable isotope, this test may be repeated as often as required. It will allow the control of therapeutic regimens and also help to unravel genetic influences in stone formation.

Adolescent↗
PubMed1998

[14C-oxalate autoradiographic studies on distribution of oxalate and calcium oxalate crystal fixation in rat kidney].

To elucidate the intrarenal distribution of oxalate and to reveal the first site of calcium oxalate crystal fixation along the nephron, we carried out 14C-oxalate renal microautoradiography by the thaw mount method 30, 60 and 90 min after intravenous administration of 14C-oxalate, in normal rats and in hyperoxaluric rats fed a vitamin B6-deficient diet for 4 and 9 weeks. In normal rats, radioactivity was observed in the entire kidney area at 30 min after the injection and at 90 min there was radioactivity only in the papilla, where radioactivity appeared in the parenchyma, mamely the epithelial cells of collecting ducts and the surrounding interstitial tissue. In hyperoxaluric rats, microautoradiograms showed the spotted deposits of 14C-oxalate in both renal papilla and medulla. In 600 x magnification of the autoradiograms, most of the deposits were detected in the epithelial cells of collecting ducts and the surrounding interstitial tissue. These deposits were identified by a polarizing microscope and X-ray microanalysis as crystal deposits of calcium oxalate. These results indicated that oxalate remained for an extended period of time in the epithelial cells of collecting ducts and in the surrounding interstitial tissue in renal papilla, and the calcium oxalate crystals fixed to the same tissue was the first step in the development of calcium oxalate stones.

Animals↗
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↗
PubMed2003

Rapid and convenient determination of oxalic acid employing a novel oxalate biosensor based on oxalate oxidase and SIRE technology.

A new method for rapid determination of oxalic acid was developed using oxalate oxidase and a biosensor based on SIRE (sensors based on injection of the recognition element) technology. The method was selective, simple, fast, and cheap compared with other present detection systems for oxalate. The total analysis time for each assay was 2-9 min. A linear range was observed between 0 and 5 mM when the reaction conditions were 30 degrees C and 60 s. The linear range and upper limit for concentration determination could be increased to 25 mM by shortening the reaction time. The lower limit of detection in standard solutions, 20 microM, could be achieved by means of modification of the reaction conditions, namely increasing the temperature and the reaction time. The biosensor method was compared with a conventional commercially available colorimetric method with respect to the determination of oxalic acid in urine samples. The urine oxalic acid concentrations determined with the biosensor method correlated well (R=0.952) with the colorimetric method.

Biosensing Techniques↗
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↗
PubMed2003

Association of absence of intestinal oxalate degrading bacteria with urinary calcium oxalate stone formation.

AIM: Urinary concentration of oxalate is considered an important factor in the formation of renal stones. Dietary oxalate is a major contributor to urinary oxalate excretion in most individuals. Furthermore, oxalate degrading bacteria have been isolated from human feces. We investigated the significance of oxalate degrading bacteria for urinary oxalate excretion and urinary stone formation. METHODS: Twenty-two known calcium oxalate stone-forming patients (stone formers) and 34 healthy volunteers (non-stone formers) were included in the study. Stool specimens were inoculated into pepton yeast glucose (PYG) medium supplemented with oxalate under anaerobic condition at 37 C for one week. After the incubation period, each colony was checked for the loss of oxalate from the culture medium. A 24-h urine sample was collected in 43 individuals and analyzed for oxalate excretion. RESULTS: Twenty-eight of 34 (82%) healthy volunteers and 10 of 22 (45%) calcium oxalate stone formers were colonized with oxalate degrading bacteria. Calcium oxalate stone formers were more frequently free of oxalate degrading bacteria (P < 0.01). Urinary excretion of oxalate in those with oxalate degrading bacteria was significantly less than in those without oxalate degrading bacteria (P < 0.05). Hyperoxaluria (> 40 mg/day) was found in four of 27 individuals (15%) with oxalate degrading bacteria compared to seven of 16 (44%) without oxalate degrading bacteria (P < 0.05), suggesting an association between the absence of oxalate degrading bacteria and the presence of hyperoxaluria. CONCLUSION: The absence of oxalate degrading bacteria in the gut could promote the absorption of oxalate, thereby increasing the level of urinary oxalate excretion. The absence of oxalate degrading bacteria from the gut appears to be a risk factor for the presence of absorptive hyperoxaluria and an increased likelihood of urolithiasis.

Adult↗
PubMed2003

Urinary oxalic acid excretion differs after oral loading of rats with various oxalate salts.

BACKGROUND: To compare urinary oxalate excretion after the oral administration of oxalic acid, disodium oxalate, or calcium oxalate in rats. METHODS: Male Wistar rats were divided into four groups of six rats each and were intravenously hydrated with normal saline, and then were administered normal saline (control group), 10 mg of oxalic acid, equimolar disodium oxalate, or equimolar calcium oxalate via a gastrostomy. Urine specimens were collected just before administration and at hourly intervals up to 5 h afterwards. The urinary oxalate, calcium, magnesium and phosphorus levels were measured. RESULTS: Urinary oxalate excretion peaked at 1-2 h after administration of oxalic acid or equimolar disodium oxalate, while administration of calcium oxalate only caused a small increase of urinary oxalate excretion. Cumulative urinary oxalate excretion during 5 h was 1.69 +/- 0.10 mg (mean +/- SD; 17%), 1.43 +/- 0.13 mg (13%), and 0.22 +/- 0.03 mg (2%) after the administration of oxalic acid, disodium oxalate, and calcium oxalate, respectively. Urinary calcium excretion showed a decrease in the oxalic acid and disodium oxalate groups, while urinary magnesium or phosphorus excretion did not change significantly. CONCLUSION: The upper gastrointestinal tract seems to be the major site of oxalic acid absorption and only free oxalate is absorbed irrespective of whether it is the sodium salt or not. After binding to calcium in the gut, oxalic acid absorption seems to be inhibited in the presence of calcium and this means that calcium oxalate is poorly absorbed (at least in the upper gastrointestinal tract).

Administration, Oral↗
PubMed2001

Contribution of dietary oxalate to urinary oxalate excretion.

BACKGROUND: The amount of oxalate excreted in urine has a significant impact on calcium oxalate supersaturation and stone formation. Dietary oxalate is believed to make only a minor (10 to 20%) contribution to the amount of oxalate excreted in urine, but the validity of the experimental observations that support this conclusion can be questioned. An understanding of the actual contribution of dietary oxalate to urinary oxalate excretion is important, as it is potentially modifiable. METHODS: We varied the amount of dietary oxalate consumed by a group of adult individuals using formula diets and controlled, solid-food diets with a known oxalate content, determined by a recently developed analytical procedure. Controlled solid-food diets were consumed containing 10, 50, and 250 mg of oxalate/2500 kcal, as well as formula diets containing 0 and 180 mg oxalate/2500 kcal. Changes in the content of oxalate and other ions were assessed in 24-hour urine collections. RESULTS: Urinary oxalate excretion increased as dietary oxalate intake increased. With oxalate-containing diets, the mean contribution of dietary oxalate to urinary oxalate excretion ranged from 24.4 +/- 15.5% on the 10 mg/2500 kcal/day diet to 41.5 +/- 9.1% on the 250 mg/2500 kcal/day diet, much higher than previously estimated. When the calcium content of a diet containing 250 mg of oxalate was reduced from 1002 mg to 391 mg, urinary oxalate excretion increased by a mean of 28.2 +/- 4.8%, and the mean dietary contribution increased to 52.6 +/- 8.6%. CONCLUSIONS: These results suggest that dietary oxalate makes a much greater contribution to urinary oxalate excretion than previously recognized, that dietary calcium influences the bioavailability of ingested oxalate, and that the absorption of dietary oxalate may be an important factor in calcium oxalate stone formation.

Adult↗
PubMed2003

Oxalate binding proteins in calcium oxalate nephrolithiasis.

The existence of several oxalate specific binding proteins have been demonstrated in human and rat kidney. These occur in both cortical and medullary cells and are distributed mostly in the subcellular organelles. About 1/3 of the total cellular oxalate binding was localised in the inner mitochondrial membrane while the rest was in the nucleus. The purified mitochondrial oxalate binding protein (62 kDa) was composed, with a higher molar proportion, of basic amino acids, and could accumulate oxalate on incorporation into liposomes. In the nucleus, histone H(1B) (27.5 kDa), nuclear membrane protein (68 kDa) and nuclear pore complex protein (205 kDa) were present with oxalate binding activities. In addition, a 45 kDa calcium oxalate binding protein was identified in most of the subcellular organelles. Both mitochondrial and nuclear oxalate binding proteins and calcium oxalate binding protein have shown the kinetic properties of specificity, saturability, pH and temperature dependency, energy of activation and inhibition by substrate analogues. All oxalate binding proteins were sensitive to the transport inhibitor 4'-4' diisothiocyano stilbene-2-2 disulphonic acid (DIDS), which is known to interact with the lysine moiety of the proteins. Calcium oxalate monohydrate (COM) crystals adsorbed oxalate binding proteins from human and rat kidney, and oxalate binding proteins isolated from human kidney stone matrix also exhibited the above kinetic properties. In experimental hyperoxaluria, all of the renal oxalate binding proteins showed enhanced oxalate binding activity with increased protein concentration. This enhanced oxalate binding activity was also attributed to increased lipid peroxidation, which correlated positively, and to decreased thiol status, which correlated negatively. A positive correlation was observed between the lipid peroxidation and both the oxalate binding activity of the in vitro peroxidised subcellular organelles and the purified protein. Similarly, in an in vivo hyperoxaluric condition, a negative correlation was observed between thiol content and both the oxalate binding activity of the peroxidised subcellular organelles and the purified protein. In the calcium oxalate crystal growth system, the oxalate binding proteins behaved either as promoters or inhibitors of the nucleation and aggregation of crystals. Following the peroxidation of the proteins, the degree of effect of the promoter protein was further stimulated while the degree of inhibition caused by the inhibitor protein further declined. Similar observations were duplicated with the proteins derived from hyperoxaluric rat kidney or kidney homogenate subjected to in vitro lipid peroxidation. The oxalate binding proteins were thought to modulate the crystallisation process in an hyperoxaluric condition similar to calcium specific binding protein modulators.

Animals↗
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↗
PubMed2000

Estimation of the oxalate content of foods and daily oxalate intake.

BACKGROUND: The amount of oxalate ingested may be an important risk factor in the development of idiopathic calcium oxalate nephrolithiasis. Reliable food tables listing the oxalate content of foods are currently not available. The aim of this research was to develop an accurate and reliable method to measure the food content of oxalate. METHODS: Capillary electrophoresis (CE) and ion chromatography (IC) were compared as direct techniques for the estimation of the oxalate content of foods. Foods were thoroughly homogenized in acid, heat extracted, and clarified by centrifugation and filtration before dilution in water for analysis. Five individuals consuming self-selected diets maintained food records for three days to determine their mean daily oxalate intakes. RESULTS: Both techniques were capable of adequately measuring the oxalate in foods with a significant oxalate content. With foods of very low oxalate content (<1.8 mg/100 g), IC was more reliable than CE. The mean daily intake of oxalate by the five individuals tested was 152 +/- 83 mg, ranging from 44 to 352 mg/day. CONCLUSIONS: CE appears to be the method of choice over IC for estimating the oxalate content of foods with a medium (>10 mg/100 g) to high oxalate content due to a faster analysis time and lower running costs, whereas IC may be better suited for the analysis of foods with a low oxalate content. Accurate estimates of the oxalate content of foods should permit the role of dietary oxalate in urinary oxalate excretion and stone formation to be clarified. Other factors, apart from the amount of oxalate ingested, appear to exert a major influence over the amount of oxalate excreted in the urine.

Adult↗
PubMed1984

[Plasma oxalate concentration in calcium oxalate stone formers].

A sensitive, simplified method for plasma oxalate determination by gas chromatography is described. After deproteinizing the plasma with 3N HC1 and 20% sulfosalicylic acid, the oxalate was methylated, extracted and analysed by gas chromatography. This method has three advantages i.e., smaller sample size (plasma 5.0 ml), rapidity (takes less than 3 hours) and accuracy. The recovery rate of oxalate added to plasma was 91.42 +/- 11.31% (SD) and the coefficient of variation of replicate determinations was 4.18%. The minimum detectable concentration of oxalate was 0.3 micrograms/ml (oxalate peak was higher than 5 mm). The mean oxalate concentration under fasting conditions from 16 healthy subjects was 1.37 +/- 0.39 micrograms/ml (SD), while that from 31 calcium oxalate stone formers was 1.45 +/- 0.39 micrograms/ml (SD). There was no significant difference in plasma oxalate concentration between the two groups. The dietary influence of oxalate on plasma and urinary oxalate was investigated in 5 healthy subjects and 5 calcium oxalate stone formers. When 100 g spinach (total oxalate 545.5 mg, soluble oxalate 381.5 mg) was given, the increase of plasma oxalate concentration was more prominent in stone formers; in stone formers it increased to 142% of control value at 2 hours (p less than 0.05) after spinach loading, to 163% at 4 hour (p less than 0.01) and to 232% at 6 hours (p less than 0.01); while in healthy subjects increased to 119% at 2 hours (ns) after loading, to 144% at 4 hours (p less than 0.05) and only to 167% at 6 hours (p less than 0.01). Urinary oxalate excretion increased promptly between 1 and 2 hours after loading in both groups, reaching peak levels between 2 and 4 hours after loading in healthy subjects and between 4 and 6 hours or later in stone formers. The mean renal clearance of oxalate was 18.0 ml/min in 6 healthy subjects and 19.0 ml/min in 4 calcium oxalate stone formers. There was no significant difference in oxalate clearance between the two groups. The mean ratio of oxalate/creatinine clearance was 0.22 for stone formers, which was equal to that for healthy subjects.

Adult↗
PubMed2000

Effects of calcium and magnesium on urinary oxalate excretion after oxalate loads.

PURPOSE: Urinary oxalate is a primary determinant of the level of calcium oxalate saturation and the formation of calcium oxalate crystals, a key event in kidney stone formation. The primary objective of this study was to compare the effects of calcium carbonate and magnesium oxide on oxalate absorption. MATERIALS AND METHODS: An experimental model was used that allowed differentiation between endogenously and oxalate load-derived urinary oxalate. Twenty-four healthy subjects (10 males, 14 females) participated in three oxalate load (OL) tests: control (OL alone), calcium carbonate (OL with concomitant calcium carbonate ingestion), and magnesium oxide (OL with concomitant magnesium oxide ingestion). Oxalate loads consisted of 180 mg. unlabeled and 18 mg. 1,2[13C2] oxalic acid. Timed urine samples were collected after the OL for analysis of oxalate, calcium, magnesium, and creatinine. RESULTS: Both the calcium carbonate and magnesium oxide treatments were associated with significantly lower load-derived oxalate levels at all time points within the initial 24-hour post-oxalate ingestion period compared with levels observed for the control treatment. There were no treatment effects on endogenous oxalate levels. The efficiency of oxalate absorption for the calcium carbonate (5.1%) and magnesium oxide (7.6%) treatments was significantly lower than that for the control treatment (13.5%). CONCLUSIONS: The results suggested that magnesium was nearly as effective as calcium in reducing oxalate absorption and urinary excretion. Higher levels of urinary oxalate, calcium, and magnesium in males appeared to be largely a function of body size since gender differences either disappeared or were reversed when a correction was made for urinary creatinine excretion.

Adult↗
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↗