Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “OXALATES”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 667 records · Page 37Linked to original sources
PubMed1985

[Effect of etidronate disodium (EHDP) on calcium oxalate renal stones induced by synthetic 1 alpha(OH) vitamin D3 and ethylene glycol in rats].

Combination of 1 alpha(OH) D3(vit D) and ethylene glycol induced renal or ureteral stones or both consisting of calcium oxalate in male Wistar rats. This study investigates the effect of EHDP on calcium oxalate stone using the rat model. EHDP reduced the frequency of renal stone and calcium content in the kidney, and reduced the size of the stones in the renal pelvis and ureter. EHDP biochemically ameliorated renal injury induced by vit D and ethylene glycol. EHDP suppressed urinary excretion of calcium even though serum calcium slightly increased. EHDP had a phosphaturic action. EHDP elevated urinary excretion of magnesium. However, the severity of hypermagnesuria decreased in the rat which was not given EHDP concomitantly. Although EHDP slightly elevated urinary excretion of oxalate in the control rat, it did not affect the high level of urinary oxalate in the vit D/ethylene glycol rat. EHDP did not produce any histological change in the kidney or femoral bone. These data indicate that EHDP can suppress renal stone formation in the vit D/ethylene glycol rat. It is speculated that firstly, EHDP may physicochemically inhibit stone formation in the process of nidus, aggregation and crystal growth of calcium oxalate, under the supersaturated condition of calcium oxalate in the urine, and secondly, EHDP may endocrinologically inhibit production of 1,25 (OH)2 vit D in the kidney or inhibit 1, 25 (OH)2 vit D-mediated intestinal calcium absorption. It is suggested that in order to prevent stone recurrence, EHDP may be clinically applied not only to calcium phosphate stones but also to calcium oxalate stones and hypercalciuria mediated by an active form of vitamin D.

Animals↗
PubMed1985

[Effect of cocoa on excretion of oxalate, citrate, magnesium and calcium in the urine of children].

Cocoa is a strong carrier of oxalic acid (average: 400 mg per 100 g). In three calcium oxalate stone formers clinical observation had been suggestive of excessive intake of cocoa products contributing to calculus formation. We studied the effect on renal oxalate excretion of an oral cocoa load (30 g per m2 body surface given on 2 consecutive days) in 12 former stone formers (group 1), 14 children with isolated microscopic haematuria (group 2), 13 healthy boys (group 3), and 12 healthy girls (group 4). A new enzymatic method was used to measure oxalic acid in cocoa products as well as in urine samples by a two step reaction: 1. Oxalate decarboxylase, 2. formiate dehydrogenase with photometry of NADH. In addition, the daily excretion of the following substances was measured: Citrate, magnesium, and calcium. There was a significant increase of urinary oxalate excretion from an average of 14.5 mg/24 hours before to an average of 22.2 mg/24 hours after the load in healthy children, and a similar increase in stone formers, but not in children with microscopic haematuria. The excretion of citrate and magnesium did not change following cocoa intake. The calcium excretion was higher in stone formers than in the other groups, but the difference was significant only compared to group 2. It is concluded that the risk of calculus formation may increase following continuous and excessive intake of cocoa products in children with a tendency toward hypercalciuria. Counselling of the stone formers resulted in a marked drop of the daily oxalate excretion, and there was no recurrence of calculus formation over a period of 6 years.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1995

Potential nephrotoxicity of intravenous infusions of naftidrofuryl oxalate.

We report two cases of acute renal failure in patients with arteriosclerosis obliterans treated by intravenous infusion of naftidrofuryl oxalate. At renal biopsy the histological lesions were identical with those found in ARF due to hyperoxaluria of other causes, revealing tubular epithelial necrosis and massive intratubular precipitation of calcium oxalate monohydrate (C1) crystals. A second study was then conducted in four other patients with arteriosclerosis obliterans to evaluate serum and urinary levels of oxalate, and crystalluria during the intravenous administration of 800 mg of naftidrofuryl oxalate per day for 10 days. During the course of treatment, the serum and urinary oxalate levels were found to increase substantially, with the gradual onset of massive C1 crystalluria. These results indicate that naftidrofuryl oxalate was responsible for the acute renal failure in the first two patients. High intravenous doses of naftidrofuryl oxalate must be used cautiously, with close surveillance of renal function.

Acute Kidney Injury↗
PubMed2005

Dissolution of kaolinite induced by citric, oxalic, and malic acids.

Kaolinite is a dominant clay mineral in the soils in tropical and subtropical regions, and its dissolution has an influence on a variety of soil properties. In this work, kaolinite dissolution induced by three kinds of low-molecular-weight organic acid, i.e., citric, oxalic, and malic acids, was evaluated under far-from-equilibrium conditions. The rates of kaolinite dissolution depended on the kind and concentration of organic acids, with the sequence R(oxalate)>R(citrate)>R(malate). Chemical calculation showed the change in concentration of organic ligand relative to change in concentration of organic acid in suspensions of kaolinite and organic acid. The effect of organic acid on kaolinite dissolution was modeled by species of organic anionic ligand. For oxalic acid, L(2-)(oxalic) and HL(-)(oxalic) jointly enhanced the dissolution of kaolinite, but for malic and citric acids, HL(-)(malic) and H2L-(citric) made a higher contribution to the total dissolution rate of kaolinite than L(2-)(malic) and L(3-)(citric), respectively. For oxalic acid, the proposed model was R(Si)=1.89x10(-12)x[(25x)/(1+25x)]+1.93x10(-12)x[(1990x1)/(1+1990x1)] (R2=0.9763), where x and x1 denote the concentrations of HL(oxalic) and L(oxalic), respectively, and x1=10(-3.81)xx/[H+]. For malic acid, the model was R(Si)=4.79x10(-12)x[(328x)/(1+328x)]+1.67x10(-13)x[(1149x1)/(1+1149x1)] (R2=0.9452), where x and x1 denote the concentrations of HL(malic) and L(malic), respectively, and x1=10(-5.11)xx/[H+], and for citric acid, the model was R(Si)=4.73x10(-12)x[(845x)/(1+845x)]+4.68x10(-12)x[(2855x1)/(1+2855x1)] (R2=0.9682), where x and x1 denote the concentrations of H2L(citric) and L(citric), respectively, and [Formula: see text] .

Journal Article↗
PubMed2005

Coadsorption of Cd(II) and oxalate ions at the TiO2/electrolyte solution interface.

The study of the adsorptions of cadmium and oxalate ions at the titania/electrolyte interface and the changes of the electrical double layer (edl) structure in this system are presented. The adsorption of cadmium or oxalate ions was calculated from an uptake of their concentration from the solution. The concentration of Cd(II) or oxalate ions in the solution was determined by radiotracer method. For labeling the solution 14C and 115Cd isotopes were used. Coadsorption of Cd(II) and oxalic ions was determined simultaneously. Besides, the main properties of the edl, i.e., surface charge density and zeta potential were determined by potentiometer titration and electrophoresis measurements, respectively. The adsorption of cadmium ions increases with pH increase and shifts with an increase of the initial concentration of Cd(II) ions towards higher pH values. The adsorption process causes an increase of negatively charged sites on anatase and a decrease of the zeta potential with an increase of initial concentration of these ions. The adsorption of oxalate anions at the titania/electrolyte interface proceeds through the exchange with hydroxyl groups. A decrease of pH produces an increase of adsorption of oxalate ions. The processes of anion adsorption lead to increase the number of the positively charged sites at the titania surface. However, specific adsorption of bidenate ligand as oxalate on one surface hydroxyl group may form inner sphere complexes on the metal oxide surface and may overcharge the compact part of the edl. The presence of oxalate ions in the system affects the adsorption of Cd(II) ions on TiO2, increasing the adsorption at low pH range and decreasing the adsorption at high pH range. Using adsorption as a function of pH data, some characteristic parameters of adsorption envelope were calculated.

Journal Article↗
PubMed2006

Real-time monitoring of the oxalate decarboxylase reaction and probing hydron exchange in the product, formate, using fourier transform infrared spectroscopy.

Oxalate decarboxylase converts oxalate to formate and carbon dioxide and uses dioxygen as a cofactor despite the reaction involving no net redox change. We have successfully used Fourier transform infrared spectroscopy to monitor in real time both substrate consumption and product formation for the first time. The assignment of the peaks was confirmed using [(13)C]oxalate as the substrate. The K(m) for oxalate determined using this assay was 3.8-fold lower than that estimated from a stopped assay. The infrared assay was also capable of distinguishing between oxalate decarboxylase and oxalate oxidase activity by the lack of formate being produced by the latter. In D(2)O, the product with oxalate decarboxylase was C-deuterio formate rather than formate, showing that the source of the hydron was solvent as expected. Large solvent deuterium kinetic isotope effects were observed on V(max) (7.1 +/- 0.3), K(m) for oxalate (3.9 +/- 0.9), and k(cat)/K(m) (1.8 +/- 0.4) indicative of a proton transfer event during a rate-limiting step. Semiempirical quantum mechanical calculations on the stability of formate-derived species gave an indication of the stability and nature of a likely enzyme-bound formyl radical catalytic intermediate. The capability of the enzyme to bind formate under conditions in which the enzyme is known to be active was determined by electron paramagnetic resonance. However, no enzyme-catalyzed exchange of the C-hydron of formate was observed using the infrared assay, suggesting that a formyl radical intermediate is not accessible in the reverse reaction. This restricts the formation of potentially harmful radical intermediates to the forward reaction.

Bacillus subtilis↗
PubMed2001

Oxalate decarboxylase requires manganese and dioxygen for activity. Overexpression and characterization of Bacillus subtilis YvrK and YoaN.

The Bacillus subtilis oxalate decarboxylase (EC ), YvrK, converts oxalate to formate and CO(2). YvrK and the related hypothetical proteins YoaN and YxaG from B. subtilis have been successfully overexpressed in Escherichia coli. Recombinant YvrK and YoaN were found to be soluble enzymes with oxalate decarboxylase activity only when expressed in the presence of manganese salts. No enzyme activity has yet been detected for YxaG, which was expressed as a soluble protein without the requirement for manganese salts. YvrK and YoaN were found to catalyze minor side reactions: oxalate oxidation to produce H(2)O(2); and oxalate-dependent, H(2)O(2)-independent dye oxidations. The oxalate decarboxylase activity of purified YvrK was O(2)-dependent. YvrK was found to contain between 0.86 and 1.14 atoms of manganese/subunit. EPR spectroscopy showed that the metal ion was predominantly but not exclusively in the Mn(II) oxidation state. The hyperfine coupling constant (A = 9.5 millitesla) of the main g = 2 signal was consistent with oxygen and nitrogen ligands with hexacoordinate geometry. The structure of YvrK was modeled on the basis of homology with oxalate oxidase, canavalin, and phaseolin, and its hexameric oligomerization was predicted by analogy with proglycinin and homogentisate 1,2-dioxygenase. Although YvrK possesses two potential active sites, only one could be fully occupied by manganese. The possibility that the C-terminal domain active site has no manganese bound and is buried in an intersubunit interface within the hexameric enzyme is discussed. A mechanism for oxalate decarboxylation is proposed, in which both Mn(II) and O(2) are cofactors that act together as a two-electron sink during catalysis.

Amino Acid Sequence↗
PubMed2003

Influence of multivitamin regimen on urinary oxalate in home parenteral nutrition patients.

BACKGROUND: High urinary oxalate levels have been associated with high ascorbic acid intakes. An alteration in the vitamin regimen for home parenteral nutrition (HPN) patients because of product discontinuation resulted in provision of 500 mg instead of 100 mg ascorbic acid per HPN day. This regimen was associated with high urinary oxalate levels. PURPOSE: To determine if a switch from a multivitamin regimen containing 500 mg to one containing 100 mg of ascorbic acid daily would reduce urinary oxalate levels. METHODS: A 24-hour urine collection for oxalate was analyzed before switching the vitamin regimen back to 100 mg ascorbic acid and repeated 2 months after the change. A paired t test was conducted to compare measurements at baseline and at 2 months. RESULTS: Overall, 18 patients completed both phases of this observational study. The initial urinary oxalate of 517 +/- 63 micromol/day decreased to 425 +/- 47 micromol/day after 2 months (p = .05). However, after applying the exclusion criteria, only 6 patients could be included. The baseline urinary oxalate of 649 +/- 106 micromol/day decreased to 391 +/- 57 micromol/day after 2 months (p = .006). CONCLUSIONS: A change in the parenteral regimen of HPN patients from 500 mg ascorbic acid to 100 mg ascorbic acid is associated with a decrease in urinary oxalate levels. This suggests that a moderate dose of parenteral ascorbic acid (100 mg/day) may limit urinary oxalate appearance in HPN patients.

Journal Article↗
PubMedDate not supplied

Isolation, purification, immobilization of oxalate oxidase and its clinical applications.

Oxalate oxidase known to catalyse the aerobic oxidation of oxalic acid into CO2 and H2O2, has been found in bacteria, fungi, mosses and some higher plants. So far, a membrane bound oxalate oxidase from Pseudomonas sp. OX-53 and a soluble oxalate oxidase from seedling plants of barley and grain sorghum has been purified to homogeneity by conventional purification methods. The enzyme has been immobilized onto insoluble support such as nylon tubing, zirconia coated alkylamine glass, polyamide membrane, CO2 gas sensing electrode, H2O2 sensor probe and polyanionic electrolyte such as ethylaminemaleic anhydride (EMA). Compared to free enzyme the immobilized enzyme showed an increase in optimum pH, decrease in Vmax and time for maximum activity, higher resistance to inhibition by NaCl but no change in Km value. The immobilized enzyme has been used in both continuous flow system and discrete assays and in enzyme electrode for determination of oxalate in urine, blood and food stuff, which is essentially required for the diagnosis and treatment of hyperoxaluria and calcium oxalate urinary stones. The degradation of endogenous oxalate in rat by immobilized oxalate oxidase has opened a new vistas in enzyme therapy of hyperoxaluria.

Enzymes, Immobilized↗
PubMed2001

The solubility of calcium oxalate in tissue culture media.

The equilibrium parameters for calcium oxalate solubility in tissue culture media were investigated because of the current interest in oxalate toxicity. The calcium selective ion electrode methodology was evaluated and calcium concentrations from potentiometric calculations were verified by d-c argon plasma emission spectroscopy. The experimental K(sp)'s at 25 degrees C for Dulbecco's modified Eagle media and McCoys 5A media are equivalent to the literature K(sp) of 2.3 x 10(-9) for low ionic strength. The equilibrium concentration products, [Ca2+] [C2O2-(4)], are ten times higher than the K(sp)'s due to the high ionic strengths of tissue culture media. At 37 degrees C, addition of soluble oxalate at the 10(-3) to 10(-4) M level causes >50% precipitation of the oxalate resulting in equilibrium oxalate concentrations of less than 6 x 10(-5) M. This relatively inexpensive selective ion technique allows the determination of oxalate concentrations in equilibrium-saturated media which are substantially less than those calculated by the amount of soluble oxalate added to the media.

Calcium↗
PubMed1994

Oxalate-induced initiation of DNA synthesis in LLC-PK1 cells, a line of renal epithelial cells.

These studies examined the effects of oxalate, a constituent of renal stones, on the growth of LLC-PK1 cells. Exposure to oxalate resulted in an initiation of DNA synthesis in serum-starved, growth-arrested cells as measured by 3H-thymidine incorporation. The effects of oxalate were comparable to those observed in response to 10% serum. Moreover, exposure to oxalate plus 10% serum stimulated DNA synthesis to a greater extent than oxalate or serum alone. These studies indicate that oxalate promotes the progression of cells from the G0/G1 to the S phase of the cell cycle. However, the increase in DNA synthesis was not always followed by an increase in cell number since high concentrations of oxalate led to a reduction in cell number.

3T3 Cells↗
PubMed1984

Effects of sodium urate and uric acid crystals on the crystallization of calcium oxalate.

Crystallization of calcium oxalate in the presence of uric acid and sodium urate crystals was analyzed in a metastable crystallization system containing calcium chloride and sodium oxalate (A), in urine highly supersaturated with respect to calcium oxalate (B), and in urine with a high level of metastable supersaturation (C). In system A uric acid crystals in concentrations up to 11.4 mMol/l did not affect calcium oxalate crystallization, neither did sodium urate during the first 6 h in concentrations below 5 mMol/l. In system B neither uric acid nor sodium urate crystals affected calcium oxalate crystallization. However, an increased rate of crystallization was observed with both uric acid and sodium urate in system C, but the effect was less pronounced than with calcium oxalate seed. Urine pre-treated with sodium urate and subsequently analyzed in system A in a concentration of 2%, gave a slightly lower inhibition of calcium oxalate crystal growth. Concerning the crystal size distribution in the same system, larger crystals were observed in several urines pre-treated with uric acid and sodium urate.

Calcium Oxalate↗
PubMed1990

Urinary oxalate and glycolate excretion in healthy infants and children.

The molar ratios of oxalate and glycolate over creatinine were determined in single urine samples of 26 infants and 27 children aged 1-5 years. In 135 children aged 5-16 years, two urine specimens were collected, one before breakfast and one at noon. Oxalate was determined by oxalate oxidase, and glycolate was measured by a colorimetric method (improved chromatotropic acid--sulphuric acid assay after prior purification by cation and anion exchanger). Both ratios (expressed in mmol/mol creatinine and analysed on a log-normal basis) were highest in infants 0-6 months old [mean oxalate 147 (95% confidence interval: 60-360), mean glycolate 175 (72-425)]. The mean oxalate ratio was 72 mmol/mol (29-174) at the age of 7-24 months, 44 (19-101) at the age of 2-5 years and 22 (12-40) in adolescents aged 16 years. Molar glycolate ratios were higher, but disclosed the same pattern. Oxalate and glycolate ratios in fasting urines did not differ significantly from those in noon samples (except glycolate in the oldest age group). Oxalate ratios correlated well with glycolate ratios in children up to 5 years of age only. Random urine samples are thus suitable for screening. However, interpretation of data requires use of age-specific reference values that are based on comparable methods.

Adolescent↗
PubMed1990

Excessive urinary oxalate excretion after combined renal and hepatic transplantation for correction of hyperoxaluria type 1.

A 4.5-year-old boy received a combined liver and kidney transplant for correction of hyperoxaluria type 1. Both organs were from the same donor and functioned primarily. Three months after transplantation, urine oxalate excretion reached a maximum of 10,500 mumol/24 h and remained above 2300 mumol/24 h for the next 2 months. Two months later, oxalate excretion decreased to about 565 mumol/24 h, indicating exhaustion of a large oxalate pool. Six months after transplantation plasma oxalate is near normal (4.9 mumol/l). With the exception of one episode of acute rejection of the renal transplant, both organs were tolerated well and continue to have a unimpaired function 9 months after transplantation. However, there is increased echogenity on renal ultrasound, indicating oxalate deposits in the grafted kidney. This case illustrates that successful combined transplantation of both liver and kidney can be performed in infants, resulting in cure of the metabolic defect. The prolonged or acute excretion of oxalate may lead to oxalate deposition in the grafted kidney without impaired graft function or early graft loss.

Child, Preschool↗
PubMed2005

Pyridoxamine lowers oxalate excretion and kidney crystals in experimental hyperoxaluria: a potential therapy for primary hyperoxaluria.

In order to prevent kidney stones and nephrolithiasis in hyperoxaluria, a new treatment that specifically reduces oxalate production and therefore urinary oxalate excretion would be extremely valuable. Pyridoxamine(PM) could react with the carbonyl intermediates of oxalate biosynthesis, glycolaldehyde and glyoxylate, and prevent their metabolism to oxalate. In PM treated rats, endogenous urinary oxalate levels were consistently lower and became statistically different from controls after 12 days of experiment. In ethylene glycol-induced hyperoxaluria, PM treatment resulted in significantly lower (by ~50%) levels of urinary glycolate and oxalate excretion compared to untreated hyperoxaluric animals, as well as in a significant reduction in calcium oxalate crystal formation in papillary and medullary areas of the kidney. These results, coupled with favorable toxicity profiles of PM in humans, show promise for the therapeutic use of PM in primary hyperoxaluria and other kidney stone diseases.

Animals↗
PubMed1990

Plasma oxalate and creatinine and oxalate/creatinine clearance ratios in normal subjects and in primary hyperoxaluria. Evidence for renal hyperoxaluria.

Plasma oxalate and creatinine were measured repeatedly in healthy individuals and in 12 patients with type 1 primary hyperoxaluria unresponsive to pyridoxine. The mean ratios were 0.025 (SD 0.006) and 0.120 (SD 0.048), respectively. One patient repeatedly had normal plasma oxalate despite markedly raised urinary oxalate and it seems unlikely that this excess oxalate could have come from the liver. Oxalate/creatinine clearance ratios in the normal group had an overall mean of 0.59 (SD 0.27) in 24 h urine collections and 0.741 (SD 0.297) in repeated short clearance periods. Both renal tubular absorption and secretion of oxalate apparently occurred on different days, but this did not depend upon urinary flow rate. Oxalate/creatinine clearance ratios in type 1 primary hyperoxaluria had a mean of 2.88 (SD 3.11). The raised oxalate/creatinine clearance ratios in the patients were not correlated with either plasma oxalate or creatinine. A few patients showed much higher clearance ratios and in some were sufficiently high to indicate that oxalate was generated and secreted in the kidneys.

Creatinine↗
PubMed1990

The formation of oxalate from glycolate in rat and human liver.

In this study, we attempted to elucidate the metabolic pathway and enzymes actually involved in oxalate formation from glycolate in rat and human liver. In rat liver, the formation of oxalate from glycolate appeared to take place predominantly via glyoxylate. The oxalate formation from glycolate observed with crude enzyme preparations was almost entirely accounted for by the sequential actions of glycolate oxidase and xanthine oxidase (XOD) or lactate dehydrogenase (LDH). Under the conditions used, no significant activity was attributable to glycolate dehydrogenase, an enzyme reported to catalyze the direct oxidation of glycolate to oxalate. Among the three enzymes known to catalyze the oxidation of glyoxylate to oxalate, glycolate oxidase and XOD showed much lower activities (a higher Km and lower Vmax) toward glyoxylate than those with the respective primary substrates. As to LDH, none of the LDH subunit-deficient patients examined showed profoundly lowered urinary oxalate excretion. Based on the results obtained, the presumed efficacies in vivo of individual enzymes, as catalysts of glyoxylate oxidation, and the in vivo conditions assumed to allow their catalysis of oxalate production are discussed.

Alcohol Oxidoreductases↗
PubMed1989

Oxalate synthesis, transport and the hyperoxaluric syndromes.

This article reviews the mechanisms involved in the synthesis, absorption, excretion and transport of oxalic acid, and the factors controlling these processes in man. The clinical syndromes associated with hyperoxaluria and recurrent calcium oxalate stone disease are reviewed, including new studies that raise the possibility of a generalized oxalate transport abnormality in some patients with renal stone disease. The important role of oxalate in the determination of calcium oxalate solubility in patients with calcium oxalate stone disease is emphasized and future directions for research in the prevention of recurrent calcium oxalate stone disease are discussed.

Animals↗