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PubMed1988

[The determination of oxalate in urine by enzymatic method using oxalate oxidase: comparison between enzymatic and gas-chromatographic methods].

Urinary oxalate is one of the most important constituents of urolithiasis, but the determination of oxalate in urine has not been performed as a routine laboratory examination. We tried to measure oxalate in urine by the enzymatic method with oxalate oxidase. The linearity of the standard curve and reproducibility of this method were confirmed. (Linearity: r = 0.996, S.D./mean: 0.5-3.6%, recovery rate: 99.5 +/- 3.3 (mean +/- S.D.)%) The correlation between this method and gas-chromatographic method was 0.926. The enzymatic method with oxalate oxidase can be utilized for determining the urinary oxalate as a routine laboratory examination.

Chromatography, Gas↗
PubMed1987

[Evaluation of the enzymatic method using oxalate oxidase for urinary oxalate assay].

The principle of this kit method is that urinary oxalate is extracted and subsequently assayed by measuring the amount of hydrogen peroxide produced in an oxidation reaction catalyzed by oxalate oxidase. The reproducibility and accuracy of the method were tested: the within-run and day-to-day coefficients of variation were 5.4-20.0% and 16.1-18.0%, respectively, and the overall recovery rate of the added oxalate (5-25 mg/l) was 40-50%. These abnormally low recovery rates may be related to the presence of sulfate and phosphate in the extracted fluid. Therefore, the above method was modified by performing a recovery test by adding 25 mg/l oxalate to all urine samples. By the modified method, the correlation coefficient obtained between this method and the ion-chromatographic method was 0.851 (p less than 0.01). Urinary pretreatment with either acid ferric chloride or EDTA yields a higher recovery than with HCl. However, a good correlation of oxalate values is consistently observed for HCl-processed urine as measured by the above two methods. If the interference of ascorbic acid is negligible, no special urinary treatment except for HCl is necessary. The 24-hour urinary oxalate excretions were 24.4 +/- 9.1 mg (mean +/- SD) in 8 healthy males and 19.9 +/- 10.3 mg in 24 calcium-stone formers (21 males and 3 females).

Adult↗
PubMed1994

[Effect of urine alkalization on excretion of renal citrate and degree of urine saturation with calcium oxalate in patients with calcium-oxalate urolithiasis and in healthy subjects].

The aim of the study was to compare the renal citrate excretion and the degree of urine saturation with calcium oxalate in patients with active calcium oxalate urolithiasis and in healthy subjects under basal conditions and after alkalization. There were 20 women before menopause with calcium stone disease aged 33.5 +/- 7.1 in the first group and 20 healthy women aged 32.3 +/- 7.6 in the second one. Sodium bicarbonate was administrated intravenously in a dose 16.8 g during 2 h. 24h excretion of calcium, magnesium and citrate, the degree of urine saturation with calcium oxalate and pH of urine before and after alkalization were evaluated. Hypocitraturia occurred in 45% of patients under basal conditions. The degree of urine saturation with calcium oxalate was significantly higher in women with nephrolithiasis (p < 0.01). A significant increase of citrate excretion (p < 0.001) and a decrease of calcium excretion (p < 0.05) after alkalization took place in both groups. The degree of urine saturation with calcium oxalate decreased significantly in patients with urolithiasis and in healthy subjects. During acute alkalosis, induced by sodium bicarbonate, increase of citrate excretion was observed in patients with urolithiasis in spite of hypocitraturia under basal conditions. This indicates that kidney function following alkalization is normal in "stone kidney". Significantly decreased saturation of urine with calcium oxalate was due to the decrease of calcium excretion and the increase of citrate excretion. In conclusion, the results show that the use of alkalizing factors in prevention of recurrent calcium urolithiasis is justifiable.

Adult↗
PubMed1989

Effect of citrate on the urinary excretion of calcium and oxalate: relevance to calcium oxalate nephrolithiasis.

Studies in 24 recurrent oxalate stone-formers have shown that values for urinary calcium excretion for this group on at-home diets vary significantly (P less than 0.001) more than values for creatinine excretions. By placing stone-formers on controlled in-hospital diets and measuring their calcium excretions, we were able to predict probable outpatient hypercalciuria (greater than 7.5 mmol/day) with a sensitivity of 95% and a specificity of 95%. In this study, the renal loss of calcium during low-calcium diets was proportional to the absorptive hypercalciuria during high-calcium diets. Calcium loading experiments in fasted stone-formers and normal subjects indicated that citrate, at citrate:calcium molar ratios ranging from 0.12 to 1, stimulated urinary calcium excretion more than did calcium carbonate loading alone. In addition, citrate also significantly (P less than 0.05) increased the excretion of urinary oxalate by two normal subjects for a given load of calcium oxalate. Malabsorption of citrate and possibly other hydroxycarboxylic acids may thus predispose to oxalate nephrolithiasis by promoting calcium and oxalate absorption.

Absorption↗
PubMed2000

Hybrid open-framework iron phosphate--oxalates demonstrating a dual role of the oxalate unit

New inorganic-organic hybrid open-framework materials of the phosphate-oxalate family, [Fe2(H2O)2-(HPO4)2(C2O4)].H2O (I), [Fe2(H2O)2-(HPO4)2(C2O4)].2H2O (II), [C3N2H12]-[Fe2(HPO4)2(C2O4)1.5]2 (III), and [C3N2OH12][Fe2(HPO4)2(C2O4)1.5]2 (IV) have been synthesized hydrothermally in the presence of structure-directing amines. The amine molecules are incorporated in III and IV, whereas I and II are devoid of them. The oxalate units act as a bridge between the layers in all the compounds. The layers in I and II are entirely inorganic, being formed by FeO6 and PO4 units, whereas in III and IV oxalate units constitute the inorganic layers and act as the bridge between these layers. Such a dual role of the oxalate unit is unique and noteworthy. The formation of two types of inorganic layers in I and II consisting of four-, six-, and eight-membered rings, indicates the interconversions between the various rings in the phosphate--oxalates to be facile. All the phosphate--oxalates show antiferromagnetic ordering at low temperatures.

Journal Article↗
PubMed2003

Early changes of oxalate and calcium urine excretion in those with calcium oxalate stone formation after extracorporeal shock wave lithotripsy.

OBJECTIVES: To determine the extent of transient changes of tubular function in idiopathic calcium-oxalate (CaOx) stone-bearing patients after extracorporeal shock wave lithotripsy (ESWL), calcium and oxalate excretion were measured before and after ESWL. METHODS: In 22 patients with renal CaOx stones, the plasma values and urine excretion of creatinine, calcium, oxalate, magnesium, and citrate were measured before and on days 1 and 2 after ESWL under conditions of a standardized diet. Overnight urine collection for an 8-hour period was used to measure the urine excretion, and the values were extrapolated to a 24-hour period. For calculation of the urine ion activity, the AP(CaOx) index EQ(s) and the CaOx risk index were used. RESULTS: After ESWL, hyperoxaluria was noted in 10 patients compared with 2 before ESWL. Hypercalciuria was seen in 11 patients after ESWL compared with 3 before. Combined hyperoxaluria and hypercalciuria was found in 7 patients after ESWL compared with 1 before. Both the oxalate/creatinine and calcium/creatinine ratios were significantly increased after ESWL. The AP(CaOx) index EQ(s) and the CaOx risk index were significantly increased after ESWL in patients with increased post-ESWL calcium and/or oxalate excretion. CONCLUSIONS: Increased calcium and/or oxalate excretion can be seen in patients with CaOx stones early after ESWL. This increased excretion of lithogenic substances represents an increased risk of fragment apposition after ESWL for the group with a significantly increased AP(CaOx) index EQ(s) and CaOx risk index. Therefore, prophylactic measures in patients at risk early after ESWL might be warranted to prevent possible recurrent stone formation.

Adult↗
PubMed2003

Lipid peroxidation and its correlations with urinary levels of oxalate, citric acid, and osteopontin in patients with renal calcium oxalate stones.

OBJECTIVES: To determine whether lipid peroxidation plays a role in patients with calcium oxalate kidney stones and to determine the correlation of lipid peroxidation with tubular damage and the major urinary risk factors. We also used the isoenzymes of glutathione S-transferase (GST) to examine which parts of the renal tubules were injured in patients with renal stones. METHODS: This clinical study included two study groups. Group 1 included 32 normal volunteers, and group 2 included 32 patients with calcium oxalate kidney stones. A 24-hour urine sample was collected from each subject, and the levels of Ca, P, Mg, oxalate, citrate, N-acetyl-beta-glucosaminidase (NAG), beta-galactosidase (GAL), alphaGST, piGST, osteopontin (OPN), thiobarbituric acid-reactive substances (TBARS), and malondialdehyde (MDA) were examined. RESULTS: Hyperoxaluria, hypocitraturia, and low urinary OPN were the major abnormalities found in the patients with stones. Elevated urinary alphaGST, NAG, and GAL were also noted in the patients with stones; however, urinary piGST showed no statistically significant difference compared with the controls. Urinary TBARS and MDA had statistically significant correlations with alphaGST, GAL, NAG, Ca, and oxalate, but had no correlation with piGST, citrate, OPN, Mg, and P. Urinary citrate had a negative, linear, and statistically significant correlation with alphaGST, GAL, and NAG. CONCLUSIONS: Lipid peroxidation correlated with hyperoxaluria and renal tubular damage, indicating that hyperoxaluria can induce tubular cell injury and that this injury may be due to the production of free radicals in patients with calcium oxalate stones. Renal tubular damage in patients with stones may be limited to the proximal tubules.

Acetylglucosaminidase↗
PubMed1981

Direct spectrophotometric determination of serum and urinary oxalate with oxalate oxidase.

A new enzymatic method for direct photometric determination of oxalate in serum and urine is described, using oxalate oxidase. The resulting H2O2 is measured with a coupled enzyme system of catalase and aldehyde dehydrogenase. Percentage recovery of added oxalate was 99 +/- 4 in serum, and 98 +/- 4 in urine (n - 10). Oxalate serum levels varied from 16.9 to 44.8 mumol/l. Oxalate values can be determined within 20 minutes, without time consuming pretreatment of samples. The detection limit is 5 mumol/l.

Aldehyde Dehydrogenase↗
PubMed1995

[The effect of the oxalate precursors on experimental calcium oxalate urolithogenesis in rats: acute and chronic administration].

Glycolate and glyoxylate, documented lithogenic precursors of oxalate, were administered acutely and chronically to Wistar-strain rats in order to study their effects on oxalate excretion and subsequent stone formation. Urinary oxalate increased significantly within 4 hours, with a maximum being reached between 4-8 hours after a single administration of glycolic acid (200 mg) or glyoxylic acid (200mg). The 24-hour increase in urinary oxalate was about 3% of each amount given. Hyperoxaluria developed immediately and persisted throughout the experimental period in all the rats, which were fed on a diet containing glycolic acid or glyoxylic acid at a 3% level. Microscopically amorphous substances accumulated in the renal tubules at one week. Significant crystal formation appeared in the tubules after two weeks in both experimental groups and consistently increased both in number and in volume until the 4th week. Therefore, the oral administration of either glycolate or glyoxylate increased urinary oxalate comparably much within a few hours, but a few weeks of hyperoxaluria may be necessary to develop crystals in the convoluted tubules.

Administration, Oral↗
PubMed1992

Reduction of urinary oxalate by combined calcium and citrate administration without increase in urinary calcium oxalate stone formers.

Oxalic acid seems to play a far greater role in the formation of calcium oxalate stone than calcium. Three grams of calcium lactate and 3 g of sodium potassium citrate were administered to 46 urolithiasis patients, whose stones were mainly composed of calcium oxalate. Urinary oxalate level was reduced significantly without raising urinary calcium level by the administration of the two drugs for two weeks. The reduction of urinary oxalic acid was particularly remarkable in patients without hypercalciuria. The mechanism of action of these drugs was discussed.

Adult↗
PubMedDate not supplied

Oxalate and calcium oxalate crystals are injurious to renal epithelial cells: results of in vivo and in vitro studies.

Calcium oxalate (CaOx) nephrolithiasis was induced in male Sprague-Dawley rats by administration of 0.75% ethylene glycol. Urinary excretion of lactate dehydrogenase (LDH) was used as a marker of cellular injury. Lipid peroxides (LP), as marker for free radical injury, were measured as malondialdehyde (MDA) in urine and the kidneys. Urinary oxalate (Ox), LDH, LP, CaOx crystals, and renal LP and CaOx crystal deposits were examined on day 0, 5, 30 and 60 of the experiment. There were significant differences between control and experimental rats in all the parameters except LDH which did not show a significant increase after 15 days. Subconfluent cultures of MDCK and LLCPK1 cells were exposed to various concentrations of oxalate and/or 500 fg/ml CaOx crystals. Cell viability was assayed by trypan blue exclusion, cellular injury was determined by measuring LDH in the media, and free radical injury was measured as MDA contents of the cells. On exposure to both Ox and/or CaOx crystals trypan blue exclusion decreased and LDH and MDA increased significantly in both tissue cultures. LLC-PK1 appeared more sensitive. The results indicate that both oxalate and calcium oxalate crystals are injurious to renal epithelial cells in the kidneys as well as in culture.

Animals↗
PubMed1982

Conductivometric determination of urinary oxalate with oxalate decarboxylase.

An enzymatic method for determination of urinary oxalate is described: the acidified urine samples are extracted with chloroform. This manipulation improves the blank values considerably. 1 ml of extracted urine is incubated with oxalate decarboxylase. The CO2 released from the medium is absorbed by Sr(OH)2. The change in conductivity measured in the Sr(OH)2 solution is linearly proportional to the oxalate concentration in urine and the method is specific for oxalate. The mean recovery is 93.2 +/- 2.5%. The coefficient of variation calculated from 28 determinations is 12.6%. The detection limit is 35 nmol. 1 ml of urine is usually sufficient for determination. The mean 24 h urine oxalate excretion of 11 healthy men and 16 women was 240 +/- 20 mumol.

Carboxy-Lyases↗
PubMed1976

A contribution to the formation mechanism of calcium oxalate urinary calculi. III. On the role of magnesium in the formation of oxalate calculi.

The influence of magnesium in vitro on the precipitation of calcium oxalate was investigated. Even at maximum physiological magnesium concentrations a litholytic effect could not be observed, but the retardation of the calcium oxalate crystallization caused by magnesium might be decisive for a reduction in calculi formation. The enlargement of the calcium oxalate crystals and aggregates caused by the retardation of crystallization, however, should be regarded as a contraindicating factor for Mg therapy in oxalate calculous disease. It is safe to say that high magnesium concentrations prevent the conversion into Whewellite of the calcium oxalate calculi substance primarily formed as Weddellite.

Calcium↗
PubMed1984

Determination of plasma oxalate with oxalate oxidase.

A method for the determination of plasma oxalate using oxalate oxidase (EC 1.2.3.4) and deproteinised plasma is described. Reference values are 1.2-6.4 mumol/l (n = 24, mean +/- SD 3.3 +/- 1.5 mumol/l). The sensitivity is 6-7 nmol, the accuracy 3-5 nmol, and the coefficient of variation 10.4% (at a level of 23 nmol). The recovery from plasma spiked with oxalate was 105 +/- 8% (n = 8). Allowing blood to stand for 4 h at room temperature had no effect on plasma oxalate levels; inhibitors of glyoxylate converting enzymes interfered with oxalate oxidase.

Humans↗
PubMed1990

Modifications to commercial oxalate oxidase based determination of urinary oxalate: a method suitable for routine clinical analysis.

A commercially available assay (Sigma) for urinary oxalates based on the oxalate oxidase/peroxidase catalyzed reaction produced, in our hands, recoveries of added oxalate that varied from patient to patient. A modification of the assay is reported that involves the chromatographic separation of interfering substances, such as ascorbate and uric acid, from oxalate prior to analysis. With the modification recoveries of added oxalate were essentially complete and showed less patient-to-patient variability. Correlation with an alternate procedure was greatly improved.

Humans↗
PubMed1994

Amperometric determination of oxalate in plasma and urine by liquid chromatography with immobilized oxalate oxidase.

A detection system for plasma and urinary oxalate involving a postcolumn enzymatic reaction and electrochemical detection is described. Oxalate oxidase was immobilized on AF-Tresyl Toyopearl 650 gel. The immobilized oxalate oxidase was packed into a stainless-steel column (10 x 4 mm I.D.) and used on-line as an immobilized enzyme reactor (IMER). The hydrogen peroxide produced by enzymatic reaction was detected amperometrically at a platinum electrode maintained at +0.5 V vs. Ag/AgCl. The HPLC separation of oxalate was carried out using a Capcell Pak C8 column and an isocratic mobile phase containing 80 mM KH2PO4 and 5 mM tetra-n-butylmammonium phosphate as an ion-pair reagent. The IMER was active and stable in the mobile phase employed. The plot of peak height against concentration of oxalate was linear in the range 0.1-1.6 mumol/ml with a correlation coefficient of 0.9989. The detection limit was 10 nmol/ml at a signal-to-noise ratio of 3. The within-day and between-day coefficients of variation were 5.3 and 7.9%, respectively.

Chromatography, High Pressure Liquid↗
PubMed1998

Mass spectrometric-selected ion monitoring assay for an oxalate absorption test applying [13C2]oxalate.

In order to assess the significance of the intestinal absorption of oxalate from food for the hyperoxaluria of the individual patient, an oxalate absorption test has been developed using doubly 13C-labelled oxalate and a gas chromatographic selected ion monitoring mass spectrometric assay. This test has been applied to volunteers and patients with urinary stones. The percentage of dose absorbed (range 1-48%) could be determined with a coefficient of variation of 15.2%. The assay to measure doubly 13C-labelled oxalate in the presence of unlabelled oxalate in urine, using the homologue malonic acid as internal standard, is described.

Carbon Isotopes↗
PubMed1999

Uric acid-binding proteins in calcium oxalate stone formers and their effect on calcium oxalate crystallization.

OBJECTIVES: To study the effect of urinary uric acid-binding proteins of controls and stone formers on calcium oxalate crystal nucleation and aggregation. MATERIALS AND METHODS: Urine samples were collected over 24 h from 20 stone formers and from 20 age-matched normal controls. Uric acid crystallization was induced by adding equal volumes of 2.5 mmol/L uric acid. The bound proteins were separated on a cellulose column, and by sodium dodecyl sulphate-polyacrylamide gel electrophoresis. The effect of the separated fractions on calcium oxalate crystal nucleation and aggregation was assessed. RESULTS: The protein bound to unit mass of uric acid crystals was higher in hyperoxaluric urine than in control urine. On cellulose-column separation, the uric acid-crystal binding proteins produced three major protein peaks, i.e. fraction I (buffer), fraction II (0.05 mol/L sodium chloride in Tris-HCl buffer) and fraction III (0.3 mol/L sodium chloride in buffer), with a minor peak obtained on elution with increasing concentrations of sodium chloride in Tris-HCl buffer (pH 7.0). Fraction I derived from either stone formers or controls promoted calcium oxalate crystallization. Fraction II from the control samples was a strong inhibitor, whereas hyperoxaluric fraction II was less inhibitory. CONCLUSION: Uric acid-binding proteins isolated either from the urine of stone formers or controls modulated calcium oxalate crystal growth. Proteins isolated from stone formers were less inhibitory of crystal nucleation and aggregation. These proteins may act as a bridge, leading to the epitaxial deposition of calcium oxalate over a urate core.

Calcium Oxalate↗