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PubMed2004

Serum oxalate in human beings and rats as determined with the use of ion chromatography.

Previous enzymatic determinations have suggested that serum oxalate concentrations in normal rats, the main animal model used in urolithiasis research, to be 3 to 5 times greater than those in healthy human subjects. In this report we validated this observation using a different method (ion chromatography) on serum samples from healthy rats and human subjects that were prepared and handled similarly. Oxalate recoveries during sample preparation for ion chromatography were strongly and variably affected by ultrafiltration devices employed for sample deproteinization and after Cl(-) removal by means of ion exchange. When oxalate recoveries were accounted for, we found significant differences in serum oxalate (6 human samples, 1.47 +/- 0.15 micromol/L; and 15 rat samples, 9.88 +/- 0.91 micromol/L). We conclude that ion-chromatographic techniques confirm the differences in serum oxalate concentrations between rats and human beings measured enzymatically and that failure to account for oxalate losses during sample preparation for ion chromatography can lead to significant underestimation of serum oxalate in both species.

Animals↗
PubMed2005

Ultrasonic degradation of oxalic acid in aqueous solutions.

This paper describes the ultrasonic degradation of oxalic acid. The effects of ultrasonic power, H(2)O(2), NaCl, external gases on the degradation of oxalic acid were investigated. Reactor flask containing oxalic acid was immersed in the ultrasonic bath with water as the coupling fluid. Representative samples withdrawn were analysed by volumetric titration. Degradation degree of oxalic acid increased with increasing ultrasonic power. It was observed that H(2)O(2) has negative contribution on the degradation of oxalic acid and there was an optimum concentration of NaCl for enhancing the degradation degree of oxalic acid. Although bubbling nitrogen gave higher degradation than that for bubbling air, both gases (for 20 min before sonication and during sonication together) could not help to enhance the degradation of oxalic acid when compared with the degradation without gas passage.

Air↗
PubMed1998

An indirect method for urinary oxalate estimation.

Oxalate was first coprecipitated at pH 5 as calcium oxalate precipitate (COP) with excess calcium ions and ethanol. Interference in the COP, mainly calcium phosphate, was successfully removed by washing with 0.1 M acetic acid equilibrated with calcium oxalate monohydrate crystal. Since the calcium content of the washed COP showed a high correlation with the original oxalate concentration, both in artificial (r = 0.998, P <0.001) and real (r = 0.951, P < 0.001 for colorimetric; r = 0.982, p < 0.001 for enzymatic methods) urines, it could be used to predict indirectly the urinary oxalate concentration. The mean percentage recovery of the predicted oxalate was 98.95, S.D. = +/-4.77% (n = 6). The method is simple, reproducible and relatively precise. It therefore could be set up as a routine method of urinary oxalate assessment in general clinical laboratories.

Artifacts↗
PubMed1994

The efficacy of (L)-2-oxothiazolidine-4-carboxylate (OTC) and (L)-cysteine in reducing urinary oxalate excretion.

The effects of orally administered (L)-cysteine and (L)-2-oxothiazolidine-4-carboxylate (OTC) on urinary oxalate excretion were investigated in male Porton rats, as (L)-cysteine has been shown to form an adduct with glyoxylate in vitro. Feeding of OTC (204 +/- 1 mg. per day) for 5 days increased urinary cyst(e)ine, p < 0.001; sulphate, p < 0.001; phosphate, p < 0.05; and calcium, p < 0.05; and decreased urinary pH, p < 0.001. In addition, OTC feeding significantly decreased urinary oxalate excretion when compared with controls, p < 0.05 (delta OTC-delta Control -4.26 +/- 1.55 nmol./day/gm.). In the 5-day period after cessation of OTC feeding, all urinary parameters returned to control levels. At the completion of this recovery period there were no significant differences in any of the clinically significant plasma parameters. When fed for 22 days (191 +/- 3 mg. per day) OTC decreased urinary oxalate compared with controls, p < 0.05 (delta OTC-delta Control -9.47 +/- 4.24 nmol./day/gm.). Other urinary parameters (uric acid, magnesium, calcium, phosphate, creatinine, pH and volume) were not significantly altered by OTC feeding. Again, at the completion of this feeding period there were no significant differences in any of the clinically significant plasma parameters. (L)-cysteine feeding for 5 days (184 +/- 10 mg. per day) increased urinary sulphate, p < 0.001; and magnesium, p < 0.05, and decreased urinary pH, p < 0.001. In addition, (L)-cysteine feeding did not significantly change urinary oxalate excretion when compared with the controls (delta(L)-Cysteine-delta Control -2.94 +/- 2.14 nmol./day/gm.). However, at the completion of this feeding period, plasma urate, p < 0.02; and glucose, p < 0.05, were decreased, and plasma potassium, p < 0.01, was increased. these results indicate that orally administered OTC is effective in reducing urinary oxalate excretion without altering plasma biochemistry. It is suggested that (L)-cysteine-glyoxylate adduct formation is the mechanism by which OTC reduces urinary oxalate excretion through a reduction in endogenous oxalate production.

Animals↗
PubMed1994

Effect of high dose vitamin C on urinary oxalate levels.

The effect of high dose ascorbate on urinary oxalate levels in healthy adults was investigated using a modified ion chromatography method. Subjects ingested 1, 5 and 10 gm. supplemental ascorbate per day for 5 days, separated by 5 days of no supplementation. Urine ascorbate levels demonstrated variable increases with ascorbate supplementation. Ascorbate added directly to urine in vitro resulted in statistically significant but modest increases in measured oxalate. Addition of 5.68 mmol./l. ascorbate increased measured urinary oxalate by 36 mumol./l., implying conversion of ascorbate to oxalate during analysis. Measurement of 24-hour urinary oxalate levels with 5 and 10 gm. ascorbate per day showed similar, modest increases, which could be entirely accounted for by oxalate production during analytical procedures. Thus, no genuine increase in urinary oxalate was demonstrable despite a greatly increased ascorbate intake.

Adult↗
PubMed1992

Calcium oxalate crystallization properties in urine with different specific electrical conductivities.

The relationship between the degree of urine dilution and the risk of calcium oxalate crystallization was studied in 32 urine samples collected from stone formers and normal subjects during an 8-hour period between 10 p.m. and 6 a.m., and in 4-hour urine samples collected during 24-hour periods from 6 patients with calcium stone disease. The risk of calcium oxalate crystallization was analyzed in terms of the increase in oxalate concentration required for a standardized precipitation of crystals of calcium oxalate. The degree of urine dilution was determined with a new instrument (urimho) designed for measuring the concentration, in terms of specific electrical conductivity, in urine samples of droplet size. With this device urine concentration can be expressed in urimho values between 1 and 5. There was a good correlation between recordings of specific electrical conductivity performed with the new device and with a conventional conductivity meter. There was a statistically significant positive correlation between urimho values and calcium oxalate crystallization. Calcium oxalate crystallization greater than 1.3 was not observed in any sample with a urimho value of 2 but it was noted in 31% of the samples with urimho values greater than 2. A positive relationship was also recorded between the urine pH and the urimho level, which is noteworthy because there was an inverse relationship between urine pH and calcium oxalate crystallization. A pH greater than 6 was observed in 78% of the samples with a urimho value of 2 but it was noted in only 27% of the samples with urimho readings between 3 and 5. A considerable variation in the response in urinary flow to ingested volumes was recorded. Therefore, monitoring of urine dilution by means of a sample device like the urimho might be of great help for patients with calcium stone disease in an effort to prevent recurrent stone formation by urine dilution, provided a urimho value of less than 3 can be maintained.

Calcium↗
PubMed1988

In vitro precipitation of calcium oxalate in the presence of whole matrix or lipid components of the urinary stones.

Organic matrix of human calcium oxalate urinary stones was obtained by demineralizing with EDTA. Lipids were extracted from the EDTA-insoluble matrix by chloroform methanol treatment. The whole matrix and its total lipid extract were then incubated in a metastable solution of calcium oxalate and depletion of calcium and oxalate ions from the calcifying solution was determined. Results of our studies described here show that urinary calcium oxalate stone matrix and its total lipid contents were capable of binding calcium and oxalate ions and of catalysing calcium oxalate crystal formation from a metastable calcium oxalate solution.

Calcium Oxalate↗
PubMed1984

The kinetics of crystallization of calcium oxalate trihydrate.

The crystal growth of calcium oxalate trihydrate has been studied in supersaturated solutions at 37C under conditions in which the activities of calcium and oxalate ions were maintained constant by the potentiostatically controlled addition of titrant solutions containing these ions. It has been possible to stabilize calcium oxalate trihydrate sufficiently without transformation to the monohydrate, to establish the kinetic behavior. The rate of growth is proportional to the square of the relative supersaturation suggesting a spiral dislocation growth mechanism. Moreover, calcium oxalate trihydrate grows considerably more rapidly than does the monohydrate. Polyphosphate ion inhibits calcium oxalate monohydrate to a much greater extent than trihydrate. In the latter case, the reduction in growth rate in the presence of this ion can be interpreted in terms of a Langmuir isotherm. The stabilization of calcium oxalate trihydrate in the presence of inhibitors by preventing the formation of the transformation product, calcium oxalate monohydrate, may be an important factor in the development of renal stones.

Calcium Oxalate↗
PubMed1980

Calcium and oxalate concentrations in human renal tissue: the key to the pathogenesis of stone formation?

On the basis of what we know about urinary supersaturation and particle growth inhibitors stone formation is unlikely to start from free crystalluric particles in the renal tubule. Therefore, the object of this study is to report data on the intrarenal distribution of calcium and oxalate in man and to examine a possible relationship between calcium and oxalate concentrations in the renal tissue and stone formation. Fresh human renal tissue was obtained at operation from 7 subjects. The calcium concentrations in the papilla, medulla and cortex were measured by atomic absorption spectrophotometry. A radioenzymatic procedure was used to determine the corresponding oxalate concentrations. Significantly higher concentrations of calcium and oxalate were observed in the papilla compared to the medulla. The medulla, in turn, contained higher concentrations than the cortex. Calcium and oxalate concentrations were 6 and 25 times higher in the normal papilla than in the urine, respectively. The ion product of calcium oxalate concentrations in the human renal tissue have not been investigated, although the frequent finding of calcification in the renal papilla suggests that they may exist. The observed intrarenal calcium and oxalate concentration gradients seem to be a significant mechanism in the pathogenesis of papillary calcification and a strong indication for renal stone formation to start from fixed crystalluric particles in the papilla.

Calcium↗
PubMed2003

Oxalate deposition on asbestos bodies.

We report on a deposition of oxalate crystals on ferruginous bodies after occupational exposure to asbestos demonstrated in 3 patients. We investigated the mechanism and possible significance of this deposition by testing the hypothesis that oxalate generated through nonenzymatic oxidation of ascorbate by asbestos-associated iron accounts for the deposition of the crystal on a ferruginous body. Crocidolite asbestos (1000 microg/mL) was incubated with 500 micromol H(2)O(2) and 500 micromol ascorbate for 24 hours at 22 degrees C. The dependence of oxalate generation on iron-catalyzed oxidant production was tested with the both the metal chelator deferoxamine and the radical scavenger dimethylthiourea. Incubation of crocidolite, H(2)O(2), and ascorbate in vitro generated approximately 42 nmol of oxalate in 24 hours. Oxalate generation was diminished significantly by the inclusion of either deferoxamine or dimethylthiourea in the reaction mixture. Incubation of asbestos bodies and uncoated fibers isolated from human lung with 500 micromol H(2)O(2) and 500 micromol ascorbate for 24 hours at 22 degrees C resulted in the generation of numerous oxalate crystals. We conclude that iron-catalyzed production of oxalate from ascorbate can account for the deposition of this crystal on ferruginous bodies.

Asbestos, Crocidolite↗
PubMed1991

Oxalate transport in renal tubular cells from normal and stone-forming animals.

To investigate the cellular mechanism(s) underlying kidney stone disease, we examined oxalate uptake in suspensions of renal cortical and papillary cells derived from control and stone-forming animals. In control animals, both cortical and papillary cells exhibited a time-dependent accumulation of oxalate. This uptake was mediated both by passive diffusion and by one or more transport processes sensitive to the anion transport inhibitor, DIDS. Oxalate uptake was also markedly sensitive to extracellular pH, showing increased uptake at acidic pH outside (pHo) (6.0), and reduced uptake at alkaline pHo (8.0). In renal tubular cells from stone-forming animals, oxalate uptake was markedly altered. Uptake was significantly reduced in cortical cells, whereas it was significantly stimulated in papillary cells from the same animals. Since the observed changes in oxalate handling occurred only in stone-forming animals, it is possible that alterations in renal cell oxalate transport contribute to calcium oxalate stone formation.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed2003

Prospective study on the efficacy of a selective treatment and risk factors for relapse in recurrent calcium oxalate stone patients.

OBJECTIVE: The present study was performed to examine the efficacy of a selective treatment according to the guidelines for the prevention of recurrence in calcium oxalate stone patients and to assess risk factors for stone recurrence. METHODS: To investigate the effect of specific diagnostic and therapeutic measures, 134 recurrent calcium oxalate stone formers participated in a prospective study for two years with regular follow-ups of at least every six months. Depending on the results of analysis of 24-hour urine, nutrition record and metabolic situation, selective recommendations were given concerning diet and medication. RESULTS: Throughout the follow-up period, 57 (43%) of the patients experienced relapses. In recurrence-free patients, the significant increase in urinary volume, as well as urinary pH, potassium and citrate excretion, three indexes of compliance with alkalization, resulted in a significant decrease in the calculated risk of calcium oxalate stone formation. In patients with recurrences during follow-up, the relative supersaturation with calcium oxalate increased significantly, mainly due to the significant rise in urinary oxalate excretion exceeding the significant increases in urinary volume, pH, potassium and citrate excretion. Multiple logistic regression analysis revealed previous ESWL treatment and a history of multiple stones as independent predictors of the risk for recurrence. CONCLUSIONS: The results indicate that compliance with drinking advice and alkalization therapy was highest among both, patients with and without recurrences, compared with all other therapeutic measures. The increase in oxalate excretion is identified as the major urinary risk factor for relapse during follow-up in recurrent calcium oxalate stone disease.

Calcium Oxalate↗
PubMed1998

Oriented growth of calcium oxalate monohydrate crystals beneath phospholipid monolayers.

Oriented calcium oxalate crystals have been grown beneath phospholipid monolayers at the air-solution interface from supersaturated calcium oxalate solutions. Mature calcium oxalate crystals grown beneath zwitterionic dipalmitoylphosphatidylcholine (DPPC) monolayers exhibit the characteristic morphology of calcium oxalate monohydrate (COM) crystals with the elongated (101) crystal face preferentially oriented parallel to the plane of the monolayer. Calcium oxalate crystals grown beneath negatively-charged dimyristoylphosphatidylserine (DMPS) monolayers also show a preferential orientation with respect to the monolayer; they do not, however, exhibit the characteristic COM morphology. Raman spectroscopy strongly suggests that the crystals grown beneath either DPPC or DMPS monolayers are the monohydrate phase of calcium oxalate; therefore, differences in crystal morphology are not due to differences in the crystalline phase. Dimyristoylphosphatidylethanolamine (DMPE), dimyristoylphosphatidic acid (DMPA), eicosanoic acid (C20), and eicosanol (C20-OH) monolayers have also been studied to help elucidate the mechanisms of interaction between the lipid monolayers and the calcium oxalate crystals. We discuss the roles of lattice matching, hydrogen bonding, stereochemistry and electrostatics on crystal orientation and morphology.

1,2-Dipalmitoylphosphatidylcholine↗
PubMed1998

Metabolic effects of oxalate in the perfused rat liver.

The effects of oxalate on the metabolism of the isolated perfused rat liver were investigated. The main purpose was to verify if oxalate is also active in intact organs as demonstrated in isolated cells. The results revealed that the action of oxalate in the perfused liver resembles only partially that observed in isolated hepatocytes. In the perfused liver, oxalate inhibited gluconeogenesis from alanine, pyruvate and lactate, inhibited glycolysis and stimulated glycogenolysis. These observations confirm previous measurements with isolated hepatocytes. However, additional effects, not observed in isolated hepatocytes, were found. In the perfused liver, oxalate stimulated glucose production from dihydroxyacetone, glycerol or sorbitol. Moreover, the effects of oxalate in the perfused rat liver occurred at concentrations well above those reported for isolated hepatocytes, revealing that the compound is less toxic in the intact tissue. In vivo, the metabolic effects reported here can only be expected to occur at supra-physiological concentrations of oxalate, as in the case of a chronic renal failure.

Alanine↗
PubMed1997

Measurement of oxalate in human plasma ultrafiltrate by ion chromatography.

An improved ion chromatographic method for the measurement of oxalate in human plasma ultrafiltrate is described. Ultrafiltration was carried out using an appropriate device and procedure. Centrifugation of 0.5 ml heparin plasma at 4 degrees C for 50 min yielded water-clear ultrafiltrate in amounts allowing replicate measurements of oxalate. The specificity of the method was confirmed. The recovery of oxalate added to plasma was approximately 80%, whereas dilution of plasma, and of an oxalate-containing salt solution, resulted in falsely high values; the mechanism(s) underlying this phenomenon are insufficiently understood at present. The intra-assay precision of the method was assessed and from ten replicates of a pool plasma, the inter-assay precision from ten measurements of the same plasma on different days; the observed ranges of oxalate were 1.32-1.56 (mean 1.42) and 1.42-1.64 (mean 1.53) micromol/l, respectively. In plasma ultrafiltrate of a limited number of healthy volunteers the range of oxalate was 1.18-2.50 micromol/l, thus permitting renal oxalate handling to be studied.

Adult↗
PubMed1989

Substrate activation by malate induced by oxalate in the Ascaris suum NAD-malic enzyme reaction.

Substrate activation of the rate of the NAD-malic enzyme reaction by malate is obtained in the presence but not in the absence of oxalate. The substrate activation is a result of competition between malate and oxalate for the E.NADH complex, with malate binding to the form of the complex unprotonated at an enzyme group with a pK of 4.9 and oxalate binding preferentially to the protonated form. The off-rate for NADH from the E.NADH complex is completely rate limiting when the group with a pK of 4.9 is protonated but is only one of several rate-limiting steps when it is unprotonated [Kiick, D.M., Harris, B.G., & Cook, P.F. (1986) Biochemistry 25, 227]. The competition by malate with oxalate thus results in an overall increase in the off-rate for NADH as a result of binding to the unprotonated form of E.NADH. Consistent with the proposed mechanism, the deuterium isotope effect on V for the nonsubstrate-activating malate concentration range decreases from 1.6 in the absence of oxalate to 1.3 in the presence of a concentration of oxalate equal to its Kii. The rate equation for the oxalate-induced substrate activation by malate is derived and presented in the Appendix. Data are discussed in terms of the overall mechanism of the NAD-malic enzyme.

Animals↗
PubMedDate not supplied

Analysis of calcium, oxalate, and citrate interaction in idiopathic calcium urolithiasis in children.

The majority of urinary stones in children are composed of calcium oxalate. To investigate the interaction between urinary calcium, oxalate, and citrate as major risk factors for calcium stones formation, their 24-h urinary excretion was determined in 30 children with urolithiasis and 15 normal healthy children. The cutoff points between children with urolithiasis and healthy children, accuracy, sensitivity, and specificity for each risk factor alone as well as for all three taken together were determined. OneR and J4.8 classifiers as parts of the larger data mining software Weka, based on machine learning algorithms, were used for the determination of the cutoff points for differentiation of the children. The decision tree based on J4.8 classifier analysis of all three risk factors together proved to be the best for differentiating stone formers from normal children. In comparison to the accuracy of the differentiation after calcium and oxalate of 80% and 75.6%, respectively, the decision tree showed an accuracy of 97.8%. Even when its stability was tested by the leave-one-out cross-validation procedure, the accuracy remained at a very acceptable percentage of 93.2% correctly classified patients. J4.8 classifier analysis gave a look inside urinary calcium, oxalate, and citrate interaction. Urinary calcium excretion was shown as the most informative in discrimination of the children with urolithiasis from healthy children. However, it was shown that oxalate and citrate excretions might influence the stone formation in a subpopulation of the stone formers. In patients with low urinary calcium, a major role in lithogenesis belongs to oxalate, in some of them alone and in others in conjunction with citrate. Decreased urinary citrate excretion in the presence of increased oxalate excretion may lead to stone formation.

Adolescent↗
PubMed2002

Steady-state dissolution kinetics of aluminum-goethite in the presence of desferrioxamine-B and oxalate ligands.

This paper reports steady-state dissolution rates of synthetic low-substitution Al-goethites (mol % Al < 10) at pH 5 in the presence of the trihydroxamate siderophore, desferrioxamine B (DFO-B), and the common biological ligand, oxalate. The siderophore-promoted Fe release rate increased both with the level of Al substitution and with DFO-B concentration up to about 100 microM, after which a plateau occurred, suggesting a saturation effect from DFO-B adsorption as a precursor to dissolution. At concentrations above 200 microM, oxalate also enhanced the Fe release rate, which however was not influenced by Al substitution. For Al-goethites with mol % Al < 4, the Fe release rate in the presence of 40 microM DFO-B together with varying concentrations of oxalate was typically greater than the corresponding sum of dissolution rates in the presence of the two ligands alone. This synergism may be the combined result of the ability of oxalate to adsorb strongly at the goethite surface, thus promoting Fe release, and of the high selectivity of DFO for Fe(III). Ferric oxalate complexes formed during dissolution will likely lose Fe3+ by ligand substitution with DFO-B, leading to the production of Fe(HDFO-B)+ and uncomplexed oxalate, the latter of which, in turn, could adsorb to the goethite surface again. For Al-goethites with mol % Al > 4, synergism was not apparent, which may signal the effect of a decreased surface density of Fe-OH sites associated with Al for Fe substitution. The oxalate-promoted release rates of Al did not scale with those of Fe, indicating incongruent dissolution. However, Al release rates in the presence of DFO-B did scale approximately with those of Fe but were not affected by the concentration of siderophore. These results are consistent with the presence of Al(OH)3 inclusions in Al-goethite.

Aluminum↗