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PubMed1991

Urinary oxalate and glycolate excretion and plasma oxalate concentration.

The diagnosis of primary hyperoxaluria in young children is hampered by the lack of a reliable reference range for urinary oxalate excretion, especially in infants. We present data on urinary oxalate and glycolate excretion in 137 normal children, on the plasma oxalate concentration in 33 normal children and 53 with chronic renal failure, and on amniotic fluid oxalate concentration in 63 uncomplicated pregnancies. The urinary oxalate:creatinine molar ratios were log normally distributed: mean (range) values were less than 1 year 0.061 (0.015-0.26), 1-5 years 0.036 (0.011-0.12), 5-12 years 0.030 (0.0059-0.15), and greater than 12 years 0.013 (0.0021-0.083). Geometric mean (range) plasma oxalate concentration in the normal children was 1.53 (0.78-3.02) mumols/l and was independent of age. The mean (SD) plasma oxalate: creatinine molar ratio in these normal children and 50 with chronic renal failure was 0.033 (0.013), and was independent of age and renal function. Mean (SD) amniotic fluid oxalate concentration was 19.0 (4.3) mumols/l.

Adolescent↗

PubMed1994

Effect of renal transplantation on serum oxalate and urinary oxalate excretion.

Serum levels of oxalate are elevated in uremic patients on dialysis. The effect of living related donor kidney transplants on serum and urine oxalate levels was studied in 8 patients. Serum and urine oxalate levels were measured prior to transplant, on the day of transplant and daily for 5 days postoperatively, and the results compared to those in 11 normal subjects. All transplanted kidneys functioned immediately. Serum oxalate fell from 55 +/- 9 mumol/l (484 +/- 79 micrograms/dl) before transplant to 21 +/- 3 mumol/l (185 +/- 26 micrograms/dl) the day after transplant, and to 9 +/- 2 mumol/l (79 +/- 18 micrograms/dl) 72 h after transplant. Serum oxalate in normal subjects was 9 +/- 2 mumol/l (79 +/- 18 micrograms/dl). During the initial 24 h after transplant urine oxalate averaged 1,244 +/- 150 mumol/l (109.5 +/- 13.2 mg), but fell to levels not statistically different from normal by 72 h after transplant. Rapid clearance of oxalate after transplant leads to transient hyperoxaluria until normal levels of serum oxalate are reached.

Adult↗

PubMed1992

Effect of vitamin B6 supplementation on plasma oxalate and oxalate removal rate in hemodialysis patients.

Whether pyridoxine (B6) supplements decrease plasma oxalate concentrations in patients on maintenance dialysis is unresolved. The effect of two dose levels of B6, 0.59 mmol/day (100 mg/day) over 6 months and 4.43 mmol (750 mg) after each dialysis treatment for 4 wk, on plasma oxalate and oxalate removal rate (dialysis plus urinary excretion) was studied in patients on maintenance hemodialysis. In both studies, a control group unsupplemented with B6, who remained on their regular diet, was also studied. The vitamin B6 status of the patients was assessed by the erythrocyte glutamate pyruvate transaminase activity and index before and during supplementation. No decrease in plasma oxalate or oxalate removal rate was found in either study. The plasma oxalate and oxalate removal rates of the unsupplemented hemodialysis patients were not different from those receiving B6 either before or after supplementation. These studies demonstrate that high-dose B6 supplementation does not decrease plasma oxalate concentration in a population of hemodialysis patients.

Alanine Transaminase↗

PubMed1999

Regulatory aspects of oxalate secretion in enteric oxalate elimination.

Enteric excretion of oxalate was studied in rats with chronic renal failure (CRF) by measuring the magnitude and direction of oxalate fluxes in vitro across short-circuited preparations of distal colon in Ussing chambers. The net absorptive flux of oxalate that is characteristic of colonic tissues removed from control rats was significantly changed to a net secretory flux in CRF rats. Injecting CRF rats with a specific angiotensin II (AngII) receptor (AT1) antagonist, losartan, results in a reversal of the CRF-induced net secretory flux (-13.87+/-0.08 pmol x cm(-2) x h(-1)) to an absorptive flux (+7.32+/-3.68 pmol x cm(-2) x h(-1)) by normalizing the unidirectional fluxes of oxalate. Similarly, oxalate fluxes were normalized across CRF colonic tissues by acute, in vitro application of losartan to the serosal bathing solution. It was also possible to simulate the CRF-induced secretory flux of oxalate (Jsm) in vitro across colonic tissues removed from control rats. Serosal application of AngII at 10(-6), 10(-5), and 10(-4) M resulted in significant increases in the s-->m flux of oxalate (increasing deltaJsm = 4.06+/-1.2, 8.41+/-0.94, and 13.8+/-3.8 pmol x cm(-2) x h(-1), respectively). Taken together, these results suggest that CRF-induced oxalate secretion is at least partly mediated by AngII, which is consistent with previous findings of a twofold upregulation of AT1 receptors in CRF colonic mucosa.

Angiotensin II↗

PubMed2000

Calcium oxalate crystallization kinetics studied by oxalate-induced turbidity in fresh human urine and artificial urine.

We have studied the kinetics of oxalate-induced turbidity in fresh human urine and artificial urine. Assays are performed in 96-well plates, which allows many oxalate concentrations to be studied, repeatedly, in a short time. The metastable limit is defined in terms of the lowest oxalate concentration that gives a rate of change of attenuance significantly greater than the control. Interpretation of rates above this limit is based on ln/ln plots of initial rates against added oxalate concentration. This approach has a good theoretical basis, is well supported by our results and gives a turbidity rate index that is related to the product of the growth rate constant and a factor relating to the number and characteristics of the heteronuclei responsible for initiation of crystallization. This interpretation is posited upon the assumptions that second-order crystallization kinetics occur in unseeded urine when supersaturation exceeds the metastable limit and that aggregation during the initial phase of crystallization does not significantly contribute to changes in turbidity. Metastable limits of urine from healthy volunteers corresponded to a calcium oxalate supersaturation ratio of approx. 10. The turbidity rate index was higher in human urine than in artificial urine. The metastable limit, based on either oxalate concentration or supersaturation, for induction of calcium oxalate crystallization in normal human urine is higher than is likely to be found in normal subjects in vivo. The shape of the relationship between the metastable limit (based on oxalate concentration) and calcium concentration emphasizes the benefit of achieving a low urine calcium concentration. Comparison of the turbidity rate indices for human and artificial urine suggests that the role of nucleation promoters is more dominant than that of growth inhibitors.

Calcium↗

PubMedDate not supplied

Determination of oxalate in urine, using an amperometric biosensor with oxalate oxidase immobilized on the surface of a chromium hexacyanoferrate-modified graphite electrode.

A novel enzymatic amperometric method is described for the determination of oxalic acid in urine. An amperometric biosensor was made by immobilizing oxalate oxidase on the surface of a chromium(III) hexacyanoferrate-modified graphite electrode by using a bovine serum albumin and glutaraldehyde cross-linking procedure. The enzyme biocatalyzes oxalate decomposition in the presence of oxygen into carbon dioxide and hydrogen peroxide. The oxalate concentration, which is proportional to the amount of hydrogen peroxide, was determined amperometrically by measuring the current resulting in the reduction of hydrogen peroxide at a very low working potential (0.05 V versus the Hg ¿Hg2Cl2¿ 3M KCl electrode), which minimized the influence of the possible interferences present in human urine. All experiments were performed with succinic buffer, pH 3.8, containing 0.1M KCl and 5.4mM ethylenediaminetetraacetic acid. In an aqueous solution of pure oxalic acid, the biosensor showed good linearity in a concentration range of 2.5-100 microM without the use of a dialysis membrane. For untreated urine samples, a high correlation (R2 = 0.9949) was obtained between oxalate concentrations added to urine samples and oxalate recoveries calculated for determinations with the described oxalate biosensor.

Biosensing Techniques↗

PubMed2006

Dependence of bisphenol A photodegradation on the initial concentration of oxalate in the lepidocrocite-oxalate complex system.

To understand the degradation of endocrine disrupting chemicals (EDCs) in natural environment with existence of iron oxides and carboxylic acids, the dependence of bisphenol A (BPA) photodegradation on the initial concentration of oxalate (COX) in lepidocrocite (gamma-FeOOH) aqueous suspension was investigated under both UV and visible lights in this study. Lepidocrocite powder was home-prepared by a hydrothermal process. It was found that BPA degradation was promoted greatly in the presence of oxalate owing to the formation of lepidocrocite-oxalate complex. And there was an optimal COX, which was 2.0 and 2.4 mmol/L, under UV and visible lights, respectively. The first-order kinetic constant, k value increased 38 times from 0.17 x 10(-2) min(-1) in the absence of oxalate to 6.39 x 10(-2) min(-1) in the presence of oxalate with an optimal COX (2.0 mmol/L) under UV irradiation, and almost 306 times from 0.02 x 10(-2) min(-1) in the absence of oxalate to 6.11 x 10(-2) min(-1) in the presence of oxalate with an optimal COX (2.4 mmol/L) under visible irradiation. The BPA degradation rate increased and the first-order kinetic constants decreased with the increase in BPA initial concentration. The dependence of the variation of pH value, total-Fe and Fe2+ during the photoreaction on COX was also investigated. The pH value increased obviously with the reaction time. Total-Fe increased dramatically at the first 5 min and then decreased quickly under UV irradiation and slowly under visible irradiation. The initial concentration of oxalate is a main factor to affect BPA photodegradation in aqueous suspension under both UV and visible lights.

Benzhydryl Compounds↗

PubMed1991

[Oxalate influx rate in red blood cells in calcium oxalate nephrolithiasis].

We established a method of human red blood cell oxalate influx rate under the condition of steady state exchange. Using this method we measured the influx rate in 10 patients with recurrent calcium oxalate nephrolithiasis and in 18 controls. DIDS inhibited oxalate flux across the human red blood cell membrane. This result suggested that band 3 protein mediates oxalate transport. Oxalate influx rate depended on reaction temperature and pH of reaction buffer. Although the oxalate influx rate in 4 degrees C could not be determined under an initial condition rate, the measurable condition was in 0 degrees C of reaction temperature. Consequently we measured the oxalate influx rate under the condition of 0 degrees C reaction temperature and 20 ml volume of washing buffer. The mean oxalate influx rate was significantly higher in patients with nephrolithiasis than in controls (-1.00 +/- 0.19 vs. -0.78 +/- 0.14).

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗

PubMed1985

[The determination of oxalate in the urine by a new enzymatic method using oxalate oxidase].

Oxalate is one of the most important constituents in urine of urinary stone. But the determination of oxalate in urine has not been performed as a routine laboratory examination because of difficulty or inaccuracy in measuring oxalate in urine. We tried to measure oxalate in urine by the newly developed enzymic method with oxalate oxidase. This method is not only simple but also accurate enough. The reproducibility S.D./mean was 2.3-9.0%, the recovery rate was 95.2 +/- 4.0% (mean +/- S.D.) With this method, the normal range of urine oxalate in 24 hours was determined to be 11.8 mg-39.4 mg, the upper limit was 40 mg. By taking the regular diet which contains 500 mg of calcium and 1,000 mg of phosphorus a day, the excretion of oxalate in urine was significantly decreased in the stone formers. This suggests that the influence of the diet upon the excretion of oxalate in urine for 24 hours is important especially in stone formers.

Diet↗

PubMed1981

[Test of efficacy of an oxalate-binding anion exchanger Colestid in healthy subjects for use in idiopathic calcium-oxalate urolithiasis].

Sodium oxalate (402 mg) was administered in a single dose to 10 healthy volunteers receiving a controlled diet. Half the group received 3 times 10 g Colestid and the other half 4 times 2 g Andursil. On the 5th day the oxalate load was repeated. Urine was collected within 32 hours following oxalate application in 8 fractions. In each fraction the levels of oxalate, calcium, phosphate and uric acid were determined. The amount of oxalate, phosphate and uric acid measured in the group receiving Colestid was lower in all fractions. Peak excretions of oxalate found in unmedicated volunteers were suppressed following oxalate load. In the group receiving Andursil, only the excretion of phosphate was decreased. The results presented suggest that Colestid may be promising in the prevention of calcium-oxalate-urolithiasis.

Anion Exchange Resins↗

PubMed1993

A comparative study of erythrocyte oxalate flux rate and urinary oxalate excretion in hyperoxaluric rats.

The present study was carried out to investigate the relation between erythrocyte oxalate flux rate and the pathogenesis of calcium oxalate renal stone disease having hyperoxaluria as the main risk factor. Male albino rats were made hyperoxaluric by feeding them diets viz. vitamin B6 deficient, vitamin B6 deficient + 51.7% galactose or fructose (serving as a sole source of carbohydrate), along with their respective pair-fed controls for 4 weeks. After 28 days of feeding, oxalate excretion was in the order of vitamin B6 deficient + galactose > galactose control > vitamin B6 deficient + fructose > vitamin B6 deficient > fructose control/vitamin B6 control. Whereas, transmembrane oxalate flux rate was in the order of vitamin B6 deficient > vitamin B6 deficient + galactose > vitamin B6 deficient + fructose > vitamin B6 control > galactose control > fructose control. No significant correlation (r = 0.304) was found between the urinary oxalate excretion and erythrocyte oxalate flux rates of various groups of rats. The study indicates that increase in oxalate excretion does not concomitantly increase the transmembrane oxalate flux in red blood cells.

Alanine Transaminase↗

PubMed1995

[Oxalate: its role in lithogenesis and composition of calcium oxalate lithiasis].

UNLABELLED: A prospective study was conducted on 374 patients with urinary lithiasis, aiming to analyze the participation of oxalate in the lithogenesis and composition of the calcium oxalate calculi, alone or associated to other factors. METHODOLOGY: Metabolic urinary study of the patient and analysis of calculi with infrared spectrography and optical microscopy. RESULTS: 26.3% patients had hyperoxaluria and 77.5% of the calculi contain calcium oxalate; these are 167 cases of calcium oxalate, 110 of oxalate and calcium phosphate and 13 cases of mixed calcium oxalate and uric acid lithiasis. 43.4% patients with pure monohydrate calcium oxalate calculi have hypercalciuria, 22.6% hyperoxaluria and 19% hyperuricosuria. Dihydrated calcium oxalate calculi are related to high hypercalciuria in 65% cases and to significant hyperoxaluria in 35% cases. 45% patients present a single lithogenic factor, either hypercalciuria (49.6%), hyperoxaluria (20.6%), hyperuricosuria (13.74%), hypocitraturia (9%), urinary infection (1.5%), A.T.R. (2.25%) or acid oliguria (3%).

Calcium Oxalate↗

PubMed1990

[Diagnosis of intestinal oxalate hyperabsorption in patients with idiopathic recurrent calcium oxalate urinary calculi].

By oral administration of 14C-labelled oxalic acid (2.2 microns Ci; 2 mg), the mean enteral oxalate absorption in 24-h urines (collecting intervals 3, 3, 6, 12 h) of 19 healthy control subjects was determined to be 8.3%. It was 14.6% (alpha less than 1%) in 20 patients with recurrent idiopathic calcium-oxalate lithiasis. The differences in absorption were most marked in the first two 3-h urines. Under the test conditions described, maximum excretion of 14C oxalate had already occurred after 3 h (55%-57%); after 6 h it was about 85%, and after 12 h 95% of the total activity in the 24-h urine. In 68% of the control subjects, the oxalate absorption values were below 10%; in 32% they were less than or equal to 15%. For the group of lithiasis patients, these findings suggest a metabolic disorder of gastrointestinal origin. In 40%, the oxalate absorption rates were clearly above 15%. The test method described is simple to carry out and can be recommended for the assessment of idiopathic calcium-oxalate lithiasis.

Adult↗

PubMed2006

Continuous infusion of oxalate by minipumps induces calcium oxalate nephrocalcinosis.

It is hypothesized that oxalate plays an active role in calcium oxalate (CaOx) nephrocalcinosis and oxalate driven nephrolithiasis by interacting with the kidney. We developed an adjustable, nonprecursor, continuous infusion model of hyperoxaluria and CaOx nephrocalcinosis to investigate this hypothesis. Minipumps containing PBS or KOx (60-360 micromol/day; n = 5-7/dose) were implanted subcutaneously in male Sprague-Dawley rats on D0 and D6. Rats were killed on D13. Oxalate excretion and CaOx crystalluria were monitored by 20+4 h urine collections. Localization and content of intrarenal crystals were determined on frozen sections using polarization and microFTIR. Oxalate excretion was significantly elevated in all KOx rats (P < or = 0.005). CaOx crystalluria was most persistent in the 240-360 micromol/day KOx rats, but even 60 micromol/day KOx rats showed sporadic crystalluria. One hundred percent of KOx rats had CaOx nephrocalcinosis as confirmed by microFTIR. Most crystals were localized to the lumens of the corticomedullary collecting ducts. A few crystals are localized just under the papillar urothelium. The minipump model is the first model of hyperoxaluria to provide continuous infusion of oxalate. It permits control of the levels of hyperoxaluria, crystalluria and CaOx nephrocalcinosis. The level of sustained hyperoxaluria and CaOx nephrocalcinosis induced by treatment with 360 micromol/day KOx for 13D models the conditions frequently observed in jejunoileal bypass patients. Adjustments in the length of treatment and level of hyperoxaluria may allow this model to also be used to study the oxalate driven CaOx-nephrolithiasis common in patients with hyperoxaluria due to other causes.

Animals↗

PubMed2006

Concentrated urine and diluted urine: the effects of citrate and magnesium on the crystallization of calcium oxalate induced in vitro by an oxalate load.

Supplementation of certain calcium crystallization inhibitors, such as citrate and magnesium, and the dilution of urine with water are now considered consolidated practice for the prevention of calcium kidney stones. The aim of this study is to verify, using tried and true in vitro methods, whether the effect of these inhibitors can manifest itself in different ways depending on whether the urine is concentrated or diluted. Calcium oxalate crystallization was studied on 4-h urine of 20 male idiopathic calcium oxalate stone formers, first under low hydration conditions (non-diluted urine) and then under high hydration conditions (diluted urine). Both the diluted and the non-diluted urine samples were subjected to three types of load: (a) an oxalate concentration increment of 1.3 mmol/l only; (b) an oxalate concentration increment of 1.3 mmol/l with a citrate concentration increment of 1.56 mmol/l; (c) an oxalate concentration increment of 1.3 mmol/l with a magnesium concentration increment of 2.08 mmol/l. In non-diluted urine, the addition of the citrate and magnesium did not modify the crystallization parameters under study. In contrast, in the diluted urine the addition of the citrate and magnesium led to a reduction in the total quantity of crystals (equivalent to 35-45%) and their aggregates (equivalent to 30-40%); at the same time, there was an increase in the diameter of the monohydrate calcium oxalate crystals, which also underwent a morphological change. In conclusion, the inhibitory effects of citrate and magnesium on the crystallization of calcium oxalate do not manifest themselves in highly concentrated urine.

Calcium Oxalate↗

PubMed1986

Measurement of plasma oxalate in healthy subjects and in patients with chronic renal failure using immobilised oxalate oxidase.

A continuous flow assay using immobilised oxalate oxidase was used to measure the level of oxalate in plasma ultrafiltrate obtained from healthy subjects and from patients with chronic renal failure. The levels of oxalate in plasma from normal subjects ranged from 1.3-3.1 mumol/l (mean 2.03; SD = 0.52) with females showing a higher (p less than 0.05) level (mean 2.25 mumol/l) than males (mean 1.87 mumol/l). The mean oxalate/creatinine clearance ratio in fourteen healthy subjects was greater than unity, thus indicating a net tubular secretion of oxalate. At physiological pH, L-ascorbate was converted to oxalate in whole blood following venepuncture, in plasma and in plasma ultrafiltrate. Reduction of the spontaneous generation of oxalate in the samples prior to analysis was achieved by acidification and treatment with sodium nitrite. A linear correlation (r = 0.92; p less than 0.001) was found between plasma oxalate and plasma creatinine in patients with chronic renal failure.

Adult↗

PubMed2000

Oxalate in human seminal plasma: possible significance and problems of oxalate determination.

OBJECTIVE: To determine the level of oxalate in seminal plasma and to correlate it with andrologic variables. DESIGN: Laboratory examination. SETTING: University-based department of andrology and department of clinical chemistry. PATIENT(S): One hundred male outpatients with infertility. INTERVENTION(S): Isolated seminal plasma was stored for 120 days at -20 degrees C. MAIN OUTCOME MEASURE(S): Levels of oxalic acid in seminal plasma. RESULT(S): Oxalate levels in seminal plasma depend on the degradation of ascorbic acid to oxalic acid during storage. There was a linear nonenzymatic increase of oxalate with storage time. After 120 days of storage, the values were 133 +/- 50 micromol/L (n = 100). Oxalic acid correlated significantly with the number of sperm head anomalies, the pH value, and the age of the donors and correlated negatively with the volume of ejaculate. CONCLUSION(S): Oxalic acid in seminal plasma may influence male fertility.

Adult↗

PubMed1984

In vitro synthesis of oxalic acid has no relevant influence on plasma oxalic acid levels in haemodialysis patients.

Plasma oxalic acid concentrations were measured in 13 chronic haemodialysis patients. The mean plasma oxalic acid concentration was 128.0 +/- 48.6 mumol/l, being approximately 8 times higher than the plasma concentration of 14 volunteers (mean = 16.8 +/- 5.2 mumol/l). Ultrafiltrates obtained in vivo from these patients showed a mean oxalic acid concentration of 138.2 +/- 56.5 mumol/l. Since in vivo ultrafiltrates are free of erythrocytes and plasma enzymes, an in vitro synthesis of oxalic acid from precursors by erythrocytes and plasma enzymes can be excluded. As the oxalic acid concentration of plasma corresponded to that of in vivo ultrafiltrates, it is concluded that any in vitro formation of oxalic acid in haemodialysis patients must be negligibly small, and is irrelevant for the measurement of plasma oxalic acid levels in patients receiving regular haemodialysis.

Erythrocytes↗