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PubMed1976

Oxalate excretion during carbohydrate infusions.

Oxalate metabolism was assessed in normal rats and rats deficient in vitamins B-1 and B-6 during intravenous infusions of solutions containing glucose, fructose, sorbitol or xylitol. Urinary excretions of oxalate, glyoxylate and glycine were considerably increased in vitamin B-6 deficient rats infused with xylitol. Significant amounts of 14C-oxalate were excreted only in vitamin B-6 deficient rats infused with U 14C-xylitol. Correction of vitamin B-6 deficiency resulted in a return to normal of urinary oxalate excretion and percentage of U 14C-xylitol excreted as 14C-oxalate. The results suggest that xylitol metabolism produces an increased activity in pathways leading to oxalate formation in vitamin B-6 deficient rats.

Animals↗
PubMed1992

Combined liver kidney transplantation in primary hyperoxaluria type I. Prevention of the recidive of calcium oxalate deposits in the renal graft.

We report the case of a 31-year-old patient who underwent combined liver and kidney transplantation for primary hyperoxaluria type I. Intensive hemodialysis was performed before the intervention and post-operatively in order to maintain plasma oxalate levels near the normal range. In spite of the correction of the liver enzyme deficiency, oxalate removal from the tissular stores led to prolonged hyperoxaluria, more longer than one year after the transplantation, as already reported. This increased urinary oxalate excretion exposes the renal graft to the risk of recurrence of calcium oxalate deposits and stone formation during a prolonged period. Hemodialysis in the postoperative period and fluid intake allowing a large urine volume might be able to decrease the concentration of urinary oxalate under the critical value of 300 mumol/l, at which supersaturation of urine in respect of calcium oxalate occurs.

Adult↗
PubMedDate not supplied

A semi-micromethod for determination of oxalate in human plasma.

An enzymatic semi-micromethod for oxalate determination in human plasma was elaborated. The principle of the method depends on the oxalate isolation from deproteinized plasma, following determination by the calorimetric oxalate oxidase-peroxidase-indamine system. This method protects against internal oxalate losses and excludes an interference of contaminations. Results, obtained by this method, were reliable and ideally suited for use as real normal values (less than or equal to 6 microM) of oxalate content in the plasma of healthy individuals. The elaborated method, which can assay plasma oxalate accurately in normal individuals as well as in hyperoxalemic conditions is superior to those previously used. The procedure of semi-micromethod does not require expensive equipments and apparatus: it is simple and easy to perform in every laboratory and takes little time.

Algorithms↗
PubMed2004

[High-performance capillary electrophoresis for determination of urinary citrate and oxalate].

OBJECTIVE: To develop a method for determining urinary citrate and oxalate using high-performance capillary electrophoresis. METHODS: Capillary electrophoresis with indirect ultraviolet (UV) detection was performed for determining urinary citrate and oxalate. Sodium hromate was used as the UV-absorbing background electrolyte. RESULTS: Citrate and oxalate had a migration time of 3.76 min and 3.14 min respectively. The calibration curves were linear within a limit of about 2 microg/ml for citrate and about 1 microg/ml for oxalate. The recovery rates of citrate and oxalate were 97.53% and 99.11% respectively. CONCLUSION: This method is simple, accurate and at low cost for determining citrate and oxalate in the urine.

Citric Acid↗
PubMed2005

Effects of pre- or post-application of calcium chloride on occluding ability of potassium oxalate for the treatment of dentin hypersensitivity.

PURPOSE: To evaluate whether calcium ion supply using 1-6 mol/L CaCl2 solution could enhance the occluding ability of dentin tubules with 30% potassium oxalate treatment. METHODS: Calcium chloride solution (1-6 mol/L) was applied to dentin disks before or after application of 30% potassium oxalate solution. Occluding ability after potassium oxalate treatment was evaluated with scanning electron microscopic (SEM) observation and measurement of dentin permeability. In addition, the composition of the precipitate formed when mixing potassium oxalate and calcium chloride was analyzed with a powder x-ray diffractometer (XRD). RESULTS: SEM observations revealed that the dentin tubules were occluded homogeneously and completely with the precipitate when calcium chloride solution was applied before or after potassium oxalate treatment. However, the depth of the precipitate in dentin tubules from the dentin surface became shallower when pre-treated with calcium chloride before potassium oxalate. Although dentin permeability was greatly reduced in both groups, no significant difference could be observed between samples with and without calcium chloride application.

Adult↗
PubMed1991

Induction of oxalate binding by lipid peroxidation in rat kidney mitochondria.

Enhanced oxalate binding (150-180% of control) was observed in kidney, liver, brain and heart, after subjecting them to lipid peroxidation in presence of iron. Kidney mitochondrial oxalate binding was stimulated by different promoters, and the order of stimulation was Fe2+ greater than t-BH greater than ascorbic acid greater than Fe3+ greater than H2O2. Oxalate binding was maximum when iron concentration was between 1-2 mM. The iron-induced oxalate binding was inhibited by reduced glutathione, beta-mercaptoethanol, alpha-tocopherol and hydroxyl ion scavengers, histidine and mannitol. Catalase inhibited both Fe(2+)-H2O2 induced oxalate binding and lipid peroxidation reactions, suggesting that the induced oxalate binding in mitochondria was mediated through the hydroxyl radical reaction mechanism.

Animals↗
PubMed1991

[Alkalinizing treatment as a preventative of recurrent calcium oxalate lithiasis].

Alkalinization of urine does not dissolve calcium oxalate but simply inhibits its formation, thus reducing to a high degree the risk of crystallization, precipitation and secondary aggregation. Slight alkalinization is the most effective inhibitor of many recurrent oxalate stones. The solubility of calcium oxalate is always very low and constitutes a different issue of precipitability of oxalate radical as calcium salt which can be satisfactorily influenced by slightly alkalinizing urine. We discuss the reported results of in vitro studies, experiments in animals submitted to oxalate and ethylene glycol overload and the clinical results achieved by alkalinizing treatment of recurrent calcium oxalate stones.

Animals↗
PubMed1991

Inclusion of proteins into calcium oxalate crystals precipitated from human urine: a highly selective phenomenon.

The abundance of protein in the matrix of calcium oxalate uroliths has fueled speculation regarding its role in stone genesis. In this study, we wanted to characterize the composition of the proteins associated with early stages of calcium oxalate crystallization in urine. Calcium oxalate crystallization was induced in urine from healthy men and women by the addition of an oxalate load. The crystals were harvested and demineralized, and the proteins remaining were separated and characterized by polyacrylamide gel electrophoresis and Western blotting. Most urinary proteins were not detected in the crystals or were present in only small quantities. The most abundant urinary macromolecule, Tamm-Horsfall glycoprotein, was notably absent from the crystal extracts. The predominant protein associated with the crystals, a previously unknown urinary constituent that we call crystal matrix protein (CMP; molecular mass, 30,000 Da), was more prevalent in the crystals derived from female urine. We conclude that most urinary proteins play no direct role in calcium oxalate crystal formation. However, the protein CMP exhibits a remarkable affinity for calcium oxalate crystals and may be important in stone pathogenesis.

Blotting, Western↗
PubMed1990

Acute oxalate poisoning attributable to ingestion of curly dock (Rumex crispus) in sheep.

Ten of 100 mature ewes were afflicted with acute oxalate toxicosis within 40 hours after being temporarily penned in a lot that contained considerable growing Rumex crispus (curly dock). Clinical signs of toxicosis included excess salivation, tremors, ataxia, and recumbency. Affected ewes were markedly hypocalcemic and azotemic. Oxalate crystals were not observed in urine. Gross postmortem lesions were minimal and nondiagnostic in 2 ewes that died peracutely, but perirenal edema and renal tubular degeneration were clearly observable in ewes euthanatized on the third day of toxicosis. Diagnosis of oxalate toxicosis was confirmed by histopathologic findings. Samples of Rumex spp contained 6.6 to 11.1% oxalic acid on a dry-weight basis, a concentration comparable with that in other oxalate-containing plants that have caused acute oxalate toxicosis.

Acute Kidney Injury↗
PubMed1989

[Analysis of urinary citrate and oxalate in 42 diabetics].

Among 42 diabetics, there were 32 with the disease remaining uncontrolled after treatment. Their fasting blood glucose was 15.24 +/- 5.37 mmol/L (mean +/- S), urinary glucose 42.6 +/- 47.83 g/24 hr, urinary oxalate 0.43 +/- 0.16 mmol/24 hr and urinary citrate 3.60 +/- 2.28 mmol/24 hr All of these levels were higher than those in a control group (P less than 0.001). Urinary citrate level was significantly positively correlated with fasting blood glucose level (gamma = 0.3954, P less than 0.001). In the remaining 10 diabetics with the disease controlled after treatment the fasting blood glucose was 7.04 +/- 0.92 mmol/L, urinary citrate 1.92 +/- 0.96 mmol/24 hr and urinary oxalate 0.37 +/- 0.11 mmol/24 hr. All of these levels were significantly lower than those before treatment (P less than 0.01) and were not different from those in the control group (P greater than 0.05). This explains that urinary citrate and oxalate increased when diabetes is uncontrolled as a result of accelerated decomposition due to increased metabolism. Urinary oxalate level is correlated positively with that of urinary citrate (gamma = 0.3773, P less than 0.05). Urinary oxalate and citrate are good index reflecting diabetic metabolic changes. Analysis of urinary oxalate with ion-chromatography is accurate and rapid method worthy to be used clinically.

Adult↗
PubMed1986

Formation of calcium oxalate urolithiasis in experiment and its inhibition by pyridoxine and magnesium.

Possibility of application of experimental model of calcium oxalate urolithiasis to the study of some medicament actions useful in prevention of calcium oxalate urolithiasis in men has been examined in animal experiments. Inhibition effects of pyridoxine and magnesium in formation of calcium oxalate stone formation have been proved. Administration of pyridoxine and/or magnesium to experimental animals inhibited formation of incrustations on renal papillae. Administration of nothing but magnesium lowered considerably also frequency of nephrocalcinosis occurrence. Good reproducibility of applied model of calcium oxalate urolithiasis creates conditions for further experimental study of this kind of urolithiasis. In the previous series of experiments (4) we tiped out an experimental model of calcium oxalate urolithiasis in animals well reproducible in our conditions. In the following period we were interested, whether the created model can be applied to verification of efficiency and further study of some medicaments affecting this kind of urolithiasis. At present, pyridoxine and magnesium are mode widely used for prevention of calcium oxalate urolithiasis in the clinical practice. Therefore, we decided to use the possibilities of the evaluated experimental model for the study of their inhibition effects. The results of experiments are presented in this paper.

Animals↗
PubMed1987

Piridoxilate-associated nephrocalcinosis: a new form of chronic oxalate nephropathy.

Piridoxilate is an association of glyoxylic acid and pyridoxine in which pyridoxine is supposed to facilitate in vivo transformation of glyoxylic acid to glycine rather than to oxalic acid. However, it has recently been shown that long-term treatment with piridoxilate may result in overproduction of oxalic acid and in calcium oxalate nephrolithiasis. We report a patient in whom piridoxilate induced both oxalate nephrolithiasis and chronic oxalate nephropathy with renal insufficiency, an association that has not been previously described. Therefore, piridoxilate should be added to the list of chemicals responsible for chronic oxalate nephropathy.

Aged↗
PubMed1986

Successful treatment of hyperuricosuric calcium oxalate nephrolithiasis with potassium citrate.

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

Adult↗
PubMed1979

[Kinetics of the growth of Ca oxalate crystals from supersaturated solutions].

Several factors influencing the nucleation and growth of Ca-oxalate crystals from metastable and instable solutions were studied in some detail. Factors of interest were the absolute concentration of calcium respectively oxalate, the quotient oxalate/calcium, repeated additions of calcium and/or oxalate, the presence or absence of crystal seeds, the agitation respectively stagnation of the metastable Ca-oxalate solution, the duration of crystallization, etc. The striking findings are the eminent role of oxalate in the formation of big crystals and crystal aggregates, the distinct inhibition of crystal growth at higher and very high calcium concentrations, as well as the substantial crystal enlargement at the presistent oxalate load.

Calcium Oxalate↗
PubMed1980

Gas-chromatographic determination of urinary oxalate.

We describe a simple, rapid method for determining urinary oxalate: isolation by precipitation with calcium chloride and conversion to dimethyl oxalate, which then is measured by gas chromatography. To each sample, tracer amounts of 14C-labeled oxalic acid are added, to determine the analytical recovery of urinary oxalate. Analytical recovery of [14C]oxalic acid added to urine specimens ranged from 15 to 95% (mean, 80%), and corrected recovery, based on calculation isotope-dilution techniques, ranged from 98 to 100%. The urinary excretion of oxalic acid by 18 normal men, ages 23 to 43 years, ranged between 9 and 23 mg/24h, with a mean value of 16 mg; that by 68 patients with small-bowel bypass ranged from 60 to 210 mg/24 h, with a mean of 127 mg.

Carbon Radioisotopes↗
PubMed1980

A semi-automatic enzymic method for estimating urinary oxalate.

A two-enzyme method is presented for estimating urinary oxalate by continuous-flow analysis. Oxalate is decarboxylated, yielding formate, which is subsequently oxidized in the presence of NAD+, yielding NADH. The NADH, measured colorimetrically, is proportional to the amount of oxalate originally present in the sample. Urine is pretreated by precipitation of the oxalate and extraction of the precipitate in citrate buffer. A correction factor for the extraction efficiency is given by the recovery of [U-14C]oxalic acid added to aliquots of the 24-h urine specimen. The normal range obtained by this method was 0.20 to 0.52 mmol/24h (18 to 47 mg/24h) with a mean value of 0.37 mmol/24 h (33 mg/24h). The between-assay CV was 7.6% (n = 12), within-assay CV 3.2% (N = 25). Unlabeled oxalate (0.5 and 1.0 mol/L) added to 28 urine samples gave a mean analytical recovery of 95% (SD 10%).

Autoanalysis↗
PubMed1981

Evaluation of a routine method for determination of calcium oxalate crystal growth inhibition in diluted urine samples.

We have evaluated a routine method for determination of the inhibition of calcium oxalate crystal growth in diluted urine samples. A crystallization inhibition index is calculated from the decrease in [14C]oxalate concentration in a metastable solution of calcium chloride and sodium oxalate after addition of seed crystals of calcium oxalate. The coefficient of variation between different determinations on the same sample is less than 1.5%, and there is good correspondence between indices obtained by this method and by a more laborious older method. We also studied the influence of different urinary constituents on the crystal growth rate in the system; whereas there was significant inhibition with citrate, chondritin sulfate, and pyrophosphate, no effects were observed with ordinary urinary concentrations of calcium, magnesium, and oxalate. The mean inhibition index was lower in a group of male patients with calcium oxalate stone disease than in a control group of normal men.

Calcium Oxalate↗
PubMed1995

Evaluation of factors associated with development of calcium oxalate urolithiasis in cats.

OBJECTIVE: To evaluate dietary and environmental factors as potential risk factors for calcium oxalate urolithiasis in cats. DESIGN: Case-control study. ANIMALS: 84 cats with uroliths composed of at least 90% calcium oxalate and 258 age- and gender-matched control cats. PROCEDURE: Owners of cats with calcium oxalate urolithiasis and control cats were surveyed between November 1990 and August 1992. Owners completed a standard questionnaire administered during a single telephone interview. Data collected included information regarding signalment, environment, urination and defecation, diet, and medical history. RESULTS: Calcium oxalate uroliths tended to develop in middle- to older-aged, domestic shorthair cats of typical weight. A gender predilection was not detected. Factors associated with an increase in the risk of calcium oxalate urolithiasis in cats were feeding urine-acidifying diets, feeding a single brand of cat food without providing additional foods or table scraps, maintaining cats in an indoor-only environment, and being of the Persian breed. CLINICAL IMPLICATIONS: Control of diet and environment may help prevent calcium oxalate urolithiasis.

Age Distribution↗