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PubMed2001

Urinary oxalate excretion in female calcium oxalate stone formers with and without a history of recurrent urinary tract infections.

Therapy with antibiotics in recurrent urinary tract infections may destroy colonies of Oxalobacter formigenes in the intestinal tract. A lack of oxalate degradation caused by the absence of this bacterium is suggested to contribute to the hyperabsorption of dietary oxalate and to the increase in urinary oxalate excretion. The present study was performed to evaluate the effect of recurrent urinary tract infections and subsequent changes induced in the urinary excretion profile in female calcium oxalate stone formers. Serum biochemical profiles, 24-h urinary parameters, and the personal characteristics of 57 female calcium oxalate stone patients with recurrent urinary tract infections (RUTI) were compared with 78 female calcium oxalate stone patients without a history of urinary tract infection. All subjects were recruited during the same period. In female patients with RUTI, urinary oxalate excretion was significantly higher (0.374 mmol/day) than in females without urinary tract infection (0.308 mmol/day) (P < 0.05). Moreover, the mean 24-h pH value and urinary sodium excretion were significantly higher in women with RUTI than in women without a history of urinary tract infection. The significantly higher urinary oxalate excretion in female calcium oxalate stone formers with recurrent urinary tract infections may be associated with the application of antibiotics and a subsequent temporary or permanent decolonization of Oxalobacter formigenes.

Adult↗
PubMed1986

Degradation of oxalate in rats implanted with immobilized oxalate oxidase.

Accumulation of oxalate leads to hyperoxaluria and calcium oxalate nephrolithiasis in man. Since oxalate is a metabolic end product in mammals, the feasibility of its enzymic degradation has been tested in vivo in rats by administering exogenous oxalate oxidase. Oxalate oxidase, isolated from banana fruit peels, in its native form was found to be non-active at the physiological pH of the recipient animal. However, its functional viability in the recipient animal was ensured by its prior binding with ethylenemaleic anhydride, thus shifting its pH activity curve towards the alkaline range. Rats implanted with dialysis membrane capsules containing such immobilized oxalate oxidase in their peritoneal cavities effectively metabolized intraperitoneally injected [14C]oxalate as well as its precursor [14C]glyoxalate. The implantation of capsules containing coentrapped multienzyme preparations of oxalate oxidase, catalase and peroxidase led to a further degradation of administered [14C]oxalate in rats.

Animals↗
PubMed2003

Effects of an oxalate load on urinary oxalate excretion in calcium stone formers.

OBJECTIVE: To investigate the oxalate intake and the effect of an oxalate load on urinary oxalate excretion in calcium stone-forming (CSF) patients. DESIGN: Prospective study. SETTING: University-affiliated outpatient Renal Lithiasis Unit. PATIENTS AND CONTROLS: Seventy (70) CSF and 41 healthy subjects (HS) collected a 24-hour urine sample and were submitted to a 3-day dietary record to determine mean oxalate (Ox), calcium (Ca) and vitamin C intake. Fifty-eight (58) CSF patients were randomly selected to receive milk (N = 28) or dark (N = 30) chocolate as an oxalate load. INTERVENTION: Administration of either milk (94 mg Ox + 430 mg Ca) or dark chocolate (94 mg Ox + 26 mg Ca) for 3 days. A 24-hour urine sample was obtained before and after the load to determine calcium, oxalate, sodium, potassium, urea, and creatinine. MAIN OUTCOME MEASURE: Oxalate intake and excretion. RESULTS: CSF patients presented mean Ox intake of 98 +/- 137 mg/d, similar to that of HS (108 +/- 139 mg/d). Mean Ox and vitamin C intake was directly correlated with Ox excretion only in CSF. The consumption of dark chocolate induced a significant increase in mean urinary Ox (36 +/- 14 versus 30 +/- 10 mg/24 hr) not observed in the milk chocolate group. Thus, a 2-fold increase in Ox intake in this population of CSF patients produced a significant 20% increase in oxaluria, not observed when Ca was consumed simultaneously. CONCLUSION: The present study suggests that even small increases in Ox intake affect oxalate excretion and the mitigation of urinary oxalate increase by Ca consumption reinforces that Ca and Ox intakes for CSF patients should be in balance. Further studies are necessary to assess whether or not a 20% increase in oxaluria will lead to a higher risk of stone formation.

Adult↗
PubMed2005

Cloning and sequencing of two Ceriporiopsis subvermispora bicupin oxalate oxidase allelic isoforms: implications for the reaction specificity of oxalate oxidases and decarboxylases.

Oxalate oxidase is thought to be involved in the production of hydrogen peroxide for lignin degradation by the dikaryotic white rot fungus Ceriporiopsis subvermispora. This enzyme was purified, and after digestion with trypsin, peptide fragments of the enzyme were sequenced using quadrupole time-of-flight mass spectrometry. Starting with degenerate primers based on the peptide sequences, two genes encoding isoforms of the enzyme were cloned, sequenced, and shown to be allelic. Both genes contained 14 introns. The sequences of the isoforms revealed that they were both bicupins that unexpectedly shared the greatest similarity to microbial bicupin oxalate decarboxylases rather than monocupin plant oxalate oxidases (also known as germins). We have shown that both fungal isoforms, one of which was heterologously expressed in Escherichia coli, are indeed oxalate oxidases that possess < or =0.2% oxalate decarboxylase activity and that the organism is capable of rapidly degrading exogenously supplied oxalate. They are therefore the first bicupin oxalate oxidases to have been described. Heterologous expression of active enzyme was dependent on the addition of manganese salts to the growth medium. Molecular modeling provides new and independent evidence for the identity of the catalytic site and the key amino acid involved in defining the reaction specificities of oxalate oxidases and oxalate decarboxylases.

Alleles↗
PubMed1980

Dietary influence on serum and urinary oxalate in healthy subjects and oxalate stone formers.

With a new enzymatic method, the dietary influence of oxalate, glycine, protein, and ascorbic acid on serum and urinary oxalate has been examined. Healthy and oxalate stone-forming subjects were compared. Two doses of sodium oxalate (130 and 400 mg daily) were administered. The high dose induced significant hyperoxaluria. No changes of serum oxalate were seen. Neither glycine (4.5 g daily) nor protein (50 g daily, 50% animal protein) had any effect on serum or urinary oxalate. Urinary oxalate excretion did not increase upon ingestion of large amounts of ascorbic acid (1--6 g daily), but serum oxalate levels were significantly elevated. The value of severe dietary restrictions concerning the compounds examined here seems to be questionable, as a significant increase of urinary oxalate excretion is lacking.

Ascorbic Acid↗
PubMed1989

Plasma oxalate concentration, oxalate clearance and cardiac function in patients receiving haemodialysis.

Pre-dialysis plasma oxalate concentration was measured in a cross-sectional study of 75 patients receiving maintenance haemodialysis. The aims of this study were to enable formulation of hypotheses regarding the determinants of plasma oxalate concentration and to allow preliminary examination of the possibility that hyperoxalaemia confers an increased risk of cardiac and vascular disease even in the absence of primary hyperoxaluria. Plasma oxalate concentration ranged between 7 and 76 mumol/l, mean (SD) 34.6 (18.1) mumol/l (normal range less than 0.8-2.0 mumol/l). Significant correlations were found between plasma oxalate concentration and plasma creatinine, duration of dialysis, current dose of ascorbic acid, and serum phosphate, and each of these variables retained significance on multiple linear regression. Oxalate clearance across a 1 m2 hollow-fibre Cuprophan dialyser, at 500 ml/min dialysate flow and blood flow between 175 and 225 ml/min, was measured 1 h after commencement of dialysis (n = 19). Mean (SD) clearance was 96.5 (27.0) ml/min. No significant association was found between self-reported maximum walking distance or the occurrence of symptoms of cardiac failure and plasma oxalate concentration. No relationship was found between plasma oxalate concentration and electrocardiographic conduction disturbances (n = 8) 'major' ST/T wave changes (n = 22), 'minor' ST/T wave changes (n = 49). Plasma oxalate was significantly greater in patients with radiologically detectable calcification of medium-sized arteries than in those without calcification, but duration of dialysis was also significantly longer in these patients. Routine haemodialysis results in marked hyperoxalaemia, which may be exacerbated by ascorbate supplementation. Oxalate clearance is similar to that of other small molecules such as creatinine and phosphate.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1983

Urinary oxalate determination by use of immobilized oxalate oxidase in a continuous-flow system.

In this procedure, oxalate oxidase (EC 1.2.3.4) immobilized in a continuous-flow system is used to determine oxalate in urine. The hydrogen peroxide formed from oxalate is detected by use of a color reaction with peroxidase (EC 1.11.1.7), 3-methyl-2-benzothiazoline hydrazine, and N,N-dimethylalanine. However, urine contains an oxalate oxidase inhibitor, which cannot be removed by heating, ion-exchange resins, or cellulose columns. This makes it necessary to precipitate the oxalate before assay. The overall assay system is accurate (oxalate recovery, 95.9%), sensitive (less than or equal to 5 mumol/L), precise (within-batch CV less than 1.25%, between-batch CV less than 5%), and relatively rapid (60 samples per working day). The assay system has better accuracy than an established chemical method and a gas-chromatographic method, and is considerably less arduous than and correlates well (r = 0.94) with a modified chemical method. The reference interval for urinary oxalate excretion is 0.16-0.56 mmol per day (n = 97). Only nonphysiological concentrations of ascorbate interfere with the assay, by increasing the oxalate result in the overall assay, presumably by post-micturition formation of oxalate from ascorbate in the urine samples.

Adult↗
PubMed1983

A simple technique for assessing the propensity for crystallization of calcium oxalate and brushite in urine from the increment in oxalate or calcium necessary to elicit precipitation.

In an effort to develop a simple and reliable method with which to assess the propensity for spontaneous nucleation of calcium oxalate and brushite in urine, the permissible increment of oxalate and calcium was calculated. This represented the additional amount of oxalate or calcium that could be added to urine in three hours before spontaneous precipitation of calcium oxalate or brushite was initiated. The permissible increment of oxalate inversely correlated (P less than 0.001) with the formation-product ratio-activity-product ratio discriminant score of calcium oxalate, which was previously shown to reflect a quantitative measure of the likelihood for spontaneous nucleation. Similarly, the permissible increment of calcium inversely correlated (P less than 0.001) with the formation-product ratio-activity-product ratio discriminant score of brushite. The permissible increments in oxalate and calcium were significantly lower (P less than 0.001) in patients with renal stones than in control subjects. Moreover, treatment with thiazides, allopurinol, sodium cellulose phosphate, orthophosphate, and diphosphonate significantly raised the permissible increment of oxalate in patients with stones. Thus, the permissible increment was reliable in discriminating "stone-forming" from control urine and in assessing response to treatment.

Calcium↗
PubMed1968

Choice between autotrophy and heterotrophy in Pseudomonas oxalaticus. Utilization of oxalate by cells after adaptation from growth on formate to growth on oxalate.

1. The labelling patterns of phosphoglycerate obtained from formate-grown or oxalate-grown Pseudomonas oxalaticus after exposure for 15sec. to [(14)C]formate or [(14)C]oxalate respectively were determined. 2. The phosphoglycerate obtained from the formate-grown cells contained 78% of the radioactivity in the carboxyl group. This is in accord with that predicted for operation of the ribulose diphosphate cycle of carbon dioxide fixation. 3. The labelling pattern of the phosphoglycerate obtained from the oxalate-grown cells approached uniformity, as predicted for the heterotrophic pathway of oxalate assimilation. The departure from complete uniformity may have been due to concurrent (14)CO(2) fixation into C(4) dicarboxylic acids. 4. The labelling pattern of phosphoglycerate obtained from cells that had just started to grow on oxalate after adaptation from formate was determined after incubation of the cells for 15sec. with [(14)C]oxalate. This pattern approached uniformity. 5. The pathway of incorporation of (14)CO(2) into cells that had just started to grow on oxalate after adaptation from formate, in the presence of either formate or oxalate as energy source, was studied by chromatographic and radio-autographic analysis. 6. It is concluded from the isotopic data that a mixed heterotrophic-autotrophic metabolism, with the former mode predominating, operates in the initial stages of growth on oxalate after adaptation from growth on formate.

Journal Article↗
PubMedDate not supplied

Determination of serum oxalate using peroxyoxalate chemiluminescence of free oxalic acid.

We describe a new sensitive and specific method for determination of oxalate in human serum. By using the chemiluminescence decay of monoperoxyoxalic acid very low concentrations of oxalate (200 nmol/L) can be determined. The mean serum oxalate level in apparently healthy controls was 14.5 +/- 8.5 mumol/L. Supplementation of ascorbic acid leads to an increase in serum oxalate level. While serum oxalate concentrations of calcium oxalate stone formers (x = 16.4 +/- 9.8 mumol/L) are not significantly different from the control group, an extreme increase of serum oxalate is evident in haemodialysis patients. The serum oxalate concentration decreased during dialysis treatment from 141.4 +/- 32.1 mumol/L to 36.4 +/- 12.7 mumol/L.

Ascorbic Acid↗
PubMed2002

Interference-free sample preparation for the determination of plasma oxalate analyzed by HPLC-ER: preliminary results from calcium oxalate stone-formers and non-stone-formers.

BACKGROUND: Oxalate generation at pH-values above 5.0 and an oxalate-protein binding in acidified plasma would appear to complicate the determination of oxalate in plasma. METHODS: To avoid complex sample preparation we used a high-performance liquid chromatographic system with an inline enzyme reactor (HPLC-ER) containing immobilised oxalate oxidase. The detection limit was 0.68 micromol/l. Blood was drawn in lithium-heparin vessels and immediately centrifuged at 4 degrees C. The yielded plasma was ultrafiltered using a Centrisart-I-tube. To inhibit oxalate generation by ascorbic acid, the ultrafiltrate was acidified with 1 mol/l hydrochloric acid during ultrafiltration at 4 degrees C. The liquid thus yielded was used for HPLC-ER analysis. Blood samples were obtained from 133 healthy adults (63 men, 70 women, aged 20-94 years) with no history of renal disorder and from 79 patients (53 men, 26 women, aged 19-77 years) with a history of calcium oxalate stone formation. RESULTS: Mean plasma oxalate was 2.65 +/- 2.31 micromol/l for healthy subjects and 4.21 +/- 0.56 micromol/l for stone formers. CONCLUSIONS: Analysis yielded no significant differences between males and females. A correlation between age and plasma oxalate was found for the healthy adults (p < 0.001).

Adult↗
PubMed1997

Does urinary oxalate interfere with the inhibitory role of glycosaminoglycans and semisynthetic sulfated polysaccharides in calcium oxalate crystallization?

OBJECTIVES: Previously it was shown that the polysaccharide G872 in vitro strongly inhibits calcium oxalate monohydrate crystallization processes. However, when rats on a stone-inducing diet of ethylene glycol plus vitamin D3 are given this polysaccharide, no changes in the urine capacity for crystallization inhibition were found. We investigated here how the inhibitory action of polysaccharides changes under high oxalate conditions, as they exist in the stone inducing diet. METHODS: Calcium oxalate monohydrate (COM) crystals were incubated in a series of 0.05 M PBS buffers containing polysaccharides with increasing oxalate concentrations (0-0.4 mmol/l). The coated crystals were collected, washed and resuspended in an artificial urine. We then measured the zeta potential of the crystals, using a Coulter DELSA 440, and the initial rates for crystal growth and agglomeration, using the Coulter Multisizer II. RESULTS: Addition of oxalate to the medium shifts the negative zeta potential distribution of COM crystals coated by polysaccharides in positive direction. Particle size analysis demonstrated that the initial rates of COM crystal growth and agglomeration responding to oxalate concentration changes (0.1-->0.4 mmol/l) in the presence of G872 (0.2 mg/l) are approximately 2.5 times faster than that in the absence of G872. CONCLUSIONS: Oxalate interferes with the binding of polysaccharides to crystals. This can be envisioned to occur through changes in the crystal surface properties or by induction of functional and secondary structural changes of urinary macromolecular inhibitors such as GAGs, resulting in a decrease of their inhibitory activity against COM crystallization. Thus, in urine, a high oxalate may increase the rate of crystallization both by increasing the supersaturation and by decreasing the inhibitory potential of the urine.

Calcium Oxalate↗
PubMed2000

Discrete analysis of plasma oxalate with alkylamine glass bound sorghum oxalate oxidase and horseradish peroxidase.

We have reported a simple method of determination of plasma oxalate using a Cl(-) and NO(3)(-) insensitive oxalate oxidase purified from grain sorghum leaf and commercially available peroxidase from horseradish [Pundir et al., Ind. J. Biochem. Biophys., 35 (1998) 120-122]. The present report describes the immobilization of both the enzymes onto alkylamine glass, their kinetic properties and application for discrete analysis of plasma oxalate. In the analytic method, H(2)O(2) generated from plasma oxalate by immobilized oxalate oxidase is measured colorimetrically at 520 nm by oxidative coupling with 4-aminophenazone, and phenol catalyzed by immobilized peroxidase. The minimum detection limit of the method is 2.5 micromol/l. Analytic recovery of added oxalate in plasma was 89. 5+/-4.1% (mean+/-S.D.). The within and between day CV for plasma oxalate measurement were <9.37 and <11.0%, respectively. The normal range of plasma oxalate as measured by the present method was 3.6 to 5.7 micromol/l. The method is not only free from interference by plasma Cl(-) and NO(3)(-) but also provides the reuse of glass beads and thus reduces the cost of analysis for routine.

Adolescent↗
PubMed2001

The influence of a high-oxalate/low-calcium diet on calcium oxalate renal stone risk factors in non-stone-forming black and white South African subjects.

OBJECTIVE: To evaluate the influence of a high-oxalate/low-calcium diet on calcium oxalate stone risk factors in both black South Africans (who are largely immune to kidney stones) and white South Africans (in whom stones are more common). SUBJECTS AND METHODS: Urinary and dietary variables were examined in 11 black and 11 white South African men. None of the subjects had had a kidney stone or any metabolic illness. Their normal domestic food intake was assessed using a semiquantitative food frequency questionnaire. Subjects were given a standardized high-oxalate/low-calcium diet for 3 days; 24-h urine samples were collected before the protocol and during the final day. The samples were analysed using routine modern laboratory techniques. The urine analysis data were used to calculate the Tiselius risk index and the relative urinary supersaturations of calcium oxalate, uric acid and calcium phosphate. RESULTS: Urine analysis showed an intriguing anomaly; black subjects had significantly higher urinary pH and oxalate values than whites (6.50 vs 6.21 and 0.23 vs 0.14 mmol/24 h, respectively), while their urinary citrate was lower (1.47 vs 3.69 mmol/24 h). In addition, the Tiselius risk index and relative supersaturation of calcium oxalate were higher in black subjects. These results are contrary to those which might have been reasonably expected when comparing stone-free and stone-prone groups. After the dietary protocol, the only urinary variable which changed significantly was urinary oxalate, which increased by 57% in whites. CONCLUSION: Factors which are conventionally used to assess stone risk (pH, oxaluria, citraturia, relative supersaturation) are not helpful in identifying why South African blacks are relatively immune to stones. We suggest that relatively lower oxalate absorption rates may be a physiological feature of this racial group.

Black or African American↗
PubMed1999

Oxalic acid production by Aspergillus niger: an oxalate-non-producing mutant produces citric acid at pH 5 and in the presence of manganese.

The external pH appeared to be the main factor governing oxalic acid production by Aspergillus niger. A glucose-oxidase-negative mutant produced substantial amounts of oxalic acid as long as the pH of the culture was 3 or higher. When pH was decreased below 2, no oxalic acid was formed. The activity of oxaloacetate acetylhydrolase (OAH), the enzyme believed to be responsible for oxalate formation in A. niger, correlated with oxalate production. OAH was purified from A. niger and characterized. OAH cleaves oxaloacetate to oxalate and acetate, but A. niger never accumulated any acetate in the culture broth. Since an A. niger acuA mutant, which lacks acetyl-CoA synthase, did produce some acetate, wild-type A. niger is apparently able to catabolize acetate sufficiently fast to prevent its production. An A. niger mutant, prtF28, previously isolated in a screen for strains deficient in extracellular protease expression, was shown here to be oxalate non-producing. The prtF28 mutant lacked OAH, implying that OAH is the only enzyme involved in oxalate production in A. niger. In a traditional citric acid fermentation low pH and absence of Mn2+ are prerequisites. Remarkably, a strain lacking both glucose oxidase (goxC) and OAH (prtF) produced citric acid from sugar substrates in a regular synthetic medium at pH 5 and under these conditions production was completely insensitive to Mn2+.

Acetate-CoA Ligase↗
PubMed1996

Risk factors in urinary calcium oxalate stone formation and their relation to urinary calcium oxalate supersaturation.

BACKGROUND: We studied the effect of potential risk factors of urinary calcium oxalate saturation on calcium oxalate stone formation. METHODS: Using the Equil2 program, the DG values of calcium oxalate in 390 clinical urine specimens were estimated in 5 healthy male individuals with and without citrate therapy. RESULTS: Critical calcium-oxalate supersaturation (DG value, > 2.8) was noted in 15 out of 390 urine specimens. Of the 15, 14 late night or morning specimens had critical calcium oxalate supersaturation, while only 1 afternoon specimen was supersaturated. Critical calcium oxalate supersaturation was often associated with hyperoxaluria and hypercalciuria, while undersaturation was often associated with hypomagnesiuria, a high Ca/Mg ratio, and hypocitraturia. CONCLUSIONS: Hypomagnesiuria, hypocitraturia, and a high Ca/Mg ratio appear to be poor indicators of calcium-oxalate supersaturation, and it is hard to predict the level of calcium-oxalate saturation using single parameters.

Adult↗
PubMed1998

Determination of urinary oxalate with oxalate oxidase and peroxidase immobilized on to glass beads.

We have reported the immobilization of barley oxalate oxidase on to alkylamine glass beads through glutaraldehyde coupling (Pundir, C. S., Satyapal and Kuchhal, N. K. (1993) Clinical Chemistry 39, 1750-1751). The present report describes the immobilization of commercially available horseradish peroxidase on to zirconia-coated arylamine glass beads through diazotization and a new method for the discrete assay of urinary oxalate using both immobilized oxalate oxidase and peroxidase. In the method, urinary oxalate is precipitated with CaCl2, redissolved in HCl and then assayed using immobilized enzymes. The oxalate in 24 h urine samples from apparently healthy male adults was measured by this method and found to be in the range of 12.2-28.0 mg with a mean of 19.8 mg. The percentage recovery of added oxalate (17.5 mg/l) was 96.7 +/- 3.4 (mean +/- SD). The mean value of urinary oxalate by our method is comparable with those obtained by the Sigma kit method. The cost of oxalate determination in 100 urine samples by the present method has been compared with that of the Sigma kit method.

Biochemistry↗