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 397 records · Page 22Linked to original sources
PubMed1997

Oxalate excretion during the first 7 weeks in very-low-birth-weight infants.

To determine reference values, we studied urinary excretion of oxalate prospectively and longitudinally in a cohort of 23 very-low-birth-weight (VLBW) infants. The urinary oxalate concentrations were evaluated in 24-hour urine samples by the oxalate oxidase method. Urine samples were obtained at 1, 2-3, 4-5 and 6-7 weeks of age. The median oxalate amount was 24 mumol/kg body weight/day with a 10th-90th percentile range of 16-45 in the 1st week. Oxalate excretion was highest in 2- to 3-week-old infants (median: 35; percentile range: 26-56 mumol/kg body weight/day). In the 4th-5th week, the median was 24 (percentile range: 15-47) mumol/kg body weight/day and in weeks 6-7 also 24 (percentile range: 10-36) mumol/ kg body weight/day. Also, the urinary oxalate concentration as well as the oxalate-creatinine ratio showed increased values in the first 3 weeks of life and decreased values afterwards. In a multivariate analysis, nutrition or gestational age did not affect the urinary oxalate concentration, the daily amount excreted or the oxalate-creatinine ratio. The investigated parameters (oxalate amount and oxalate-creatinine ratio in urine) were significantly age dependent). The data show that urinary oxalate excretion in VLBW infants approaches levels that are in the same range as those of patients with urolithiasis. Thus the risk of nephrocalcinosis in VLBW infants may be increased.

Age Distribution↗
PubMed1978

Renal tubular transport of organic acids. Studies with oxalate and para-aminohippurate in the rat.

The renal handling of oxalate was examined by free-flow micropuncture, intratubular microinjection, and droplet precession techniques in the rat. After the sustained i.v. infusion of [(14)C]oxalate, the fractional delivery of oxalate from the early portions of the proximal tubule was 120.1+/-4.4%, indicating net secretion. Fractional delivery rates from the late proximal tubule (124.6+/-6.1), distal tubule (120.9+/-2.9), and final urine (126.2+/-2.9%) were not different from that of the early proximal tubule. Direct intratubular microinjections of oxalate into the early proximal tubule and late proximal tubule yielded urinary recovery rates of 85+/-3% and 101+/-2%, respectively, suggesting that oxalate absorption does occur in the mid-portions of the proximal tubule. Droplet precession studies confirmed a secretory flux for oxalate. In contrast to oxalate, para-aminohippurate (PAH), the more traditional marker for organic acid transport, was secreted in the late portions of the proximal tubule and in large measure at a site between the late proximal and distal tubules, presumably the pars recta. Probenecid inhibited PAH secretion but was without effect on net oxalate transport, oxalate absorption, or oxalate secretion. These studies demonstrate that net oxalate secretion occurs in the early portions of the proximal convoluted tubule, undergoes bidirectional transport of approximately equal magnitude in later segments of the proximal tubule, and probably is not transported in more distal nephron sites. The secretory mechanism for oxalate differs from that of PAH in that it is located in a different segment of the nephron and is not inhibited by probenecid. These differences suggest that the early portions of the proximal tubule are important in the renal metabolism of some organic acids.

Aminohippuric Acids↗
PubMed1989

Oxalate measurement in the picomol range by ion chromatography: values in fasting plasma and urine of controls and patients with idiopathic calcium urolithiasis.

Oxalate was measured by ion chromatography in the ultrafiltrate of heparinized plasma from peripheral venous blood, using a membrane with a cut-off molecular weight (Mr). The following criteria were established: sensitivity 0.7 mumol.l-1; intra- and inter-assay coefficients of variation 4% and 12%, respectively; precision of duplicate determinations (expressed as standard deviation) 0.08 mumol.l-1; overall recovery (oxalate added and diluted, respectively) 100.7%. These qualified the method for assessment of plasma oxalate in healthy human controls (males: n = 12) as well as patients with idiopathic renal calcium urolithiasis (males: n = 22; females: n = 16). Renal calcium urolithiasis patients were subclassified into those with normocalciuria and idiopathic hypercalciuria. In male and female controls the mean values (and range) of plasma oxalate were 1.98 (1.4-2.5) and 1.78 (0.7-2.9) mumol.l-1, respectively. In male controls ultrafiltration (membrane cut off Mr 10,000) revealed that 11-16% plasma oxalate was bound to constituents having an apparent Mr above 10,000, and that with use of membranes with smaller pore size, the ultrafilterability of oxalate decreases further. In renal calcium urolithiasis the following values were elicited (mumol.l-1): male normocalciuria 1.78 (0.8-4.0), idiopathic hypercalciuria 1.58 (1.2-2.2); female normocalciuria 1.69 (0.8-3.6), idiopathic hypercalciuria 1.21 (0.8-2.1). The difference from controls is significant in idiopathic hypercalciuria (males and females). In contrast, in fasting urine of renal calcium urolithiasis the oxalate excretion rate (5-45 mumol per 120 min) and oxalate clearance (21-328 ml per min) resemble those in controls, whereas in renal calcium urolithiasis the fractional oxalate clearance (30-357% of creatinine clearance) tended to higher values (p less than 0.01, in male idiopathic hypercalciuria versus controls). It is suggested that 1) ion chromatography allows the reliable assessment of ultrafiltrable plasma oxalate in health and disease states, 2) in renal calcium urolithiasis this technique may help to elucidate oxalate pathophysiology, especially the mode of renal handling of oxalate.

Adult↗
PubMed1999

Oxalate-induced changes in the viability and growth of human renal epithelial cells.

Previous studies on the porcine renal epithelial LLC-PK1 cell line demonstrated that oxalate exposure produces concentration-dependent effects on renal cell growth and viability via process(es) involving free radicals. The present studies were conducted to determine whether these findings could be extended to a renal proximal tubular epithelial cell line derived from the human kidney. These studies examined oxalate-induced changes in membrane integrity after short-term exposure (4 h) and changes in cell survival after longer-term exposure (24 to 72 h). Oxalate-induced changes were also assessed in the expression of two genes: egr-1, a zinc-finger transcription factor, and osteopontin, a protein associated with tissue remodeling. The present studies also determined whether oxalate-induced changes in either cell viability or gene expression depended on free radicals. Oxalate at a concentration > or = 175 microM (free) produced membrane damage within 4 h. This effect was inhibited by Mn(III) tetrakis (1-methyl-4-pyridyl) porphyrin (MnTMPyP), a superoxide dismutase mimetic, but not by N-acetyl cysteine, a glutathione precursor, or by deferoxamine, an iron chelator. Acute oxalate-induced injury was followed by cell loss within 24 h, an effect maintained at 48 and 72 h at high concentrations of oxalate. Oxalate also promoted DNA synthesis. This mitogenic effect offset cell loss at lower oxalate concentrations (88 microM) leading to a small but significant increase in cell number at 72 h. Treatment with oxalate also increased expression of egr-1 mRNA within 1 h, a response that was attenuated by MnTMPyP; oxalate treatment for 8 h also increased abundance of osteopontin mRNA. These studies suggest that oxalate exposure produces changes in human renal cell growth and viability via a process(es) dependent on reactive oxygen intermediates. Such changes may play a role in the development and/or progression of renal disease via generation of reactive oxygen intermediates.

Cell Division↗
PubMed2003

Clinical investigation on gastric oxalate absorption.

OBJECTIVE: To study the stomach role in exogenous oxalate absorption. METHODS: The kinetic variation of urinary oxalate excretion (mg/min) in 10 healthy adults and 8 patients who underwent total gastrectomy was investigated before and after an oral spinach oxalate load. The bioavailability of the oxalate load in the healthy adults was calculated and compared with that in the patients. RESULTS: The oxalate content in the oral spinach load was 2567-2670 mg. The urinary oxalate excretion (mg/min) in the 10 healthy adults increased significantly 20 minutes after loading (this increase was compared against their basic oxalate excretion level of 0.0331 +/- 0.0203). Further observations after loading include: a first peak of oxalate excretion 40 minutes after loading; an oxalate excretion level double that of the basic level after 60 minutes (0.0732 +/- 0.0294) and a second peak appearing at 3 hours (P < 0.01). A "first peak" (0.063% +/- 0.062%) was not in any of the patients who underwent a total gastrectomy. Furthermore, a bioavailability of oxalate, which was 50% lower than that in the healthy subjects, appeared 60 minutes after loading (0.098% +/- 0.071%, P < 0.01). CONCLUSIONS: The stomach is a powerful oxalate absorption organ under normal physiological conditions. Further investigation on the relationship between stomach dysfunction and urinary calcium oxalate formation is needed.

Absorption↗
PubMed2004

Effects of calcium supplements on the risk of renal stone formation in a population with low oxalate intake.

It has been speculated that calcium supplement in subjects with low oxalate intake might increase the risk of calcium stone formation due to an increase in calcium absorption without a significant reduction in oxalate absorption. There have been no human studies addressing specifically the effects of taking calcium supplements in populations whose dietary oxalate is low. This study was conducted to determine the effects of calcium supplements on the risk of calcium stone formation in a population with low oxalate intake. Thirty-two healthy male navy privates, 22.7 +/- 1.9 (mean +/- SD) years old, who had oxalate intake of less than 1 mmol/day, a serum creatinine of less than 150 micromol/l, and no history of renal stones, participated in the study. Dietary oxalate was controlled to be under 1 mmol/day throughout the study. Twenty-four hour urine collections for the determination of urinary constituents were obtained at baseline and after taking calcium supplements. Detection of calcium oxalate was performed to assess the risk of calcium oxalate stone formation. The urinary excretion of calcium was significantly elevated above baseline values while taking the calcium supplements (3.48 +/- 2.13 vs 5.17 +/- 2.61 mmol/d, p < 0.05) and urinary oxalate was significantly decreased when the subjects took calcium supplements compared to the corresponding baseline value (0.13 +/- 0.05 vs 0.17 +/- 0.07 mmol/d, p = 0.01). Urinary citrate was significantly elevated when the subjects took calcium supplements compared to the baseline (0.83 +/- 0.57 vs 0.64 +/- 0.39 mmol/d, p = 0.03). There was no significant alteration in the activity products of calcium oxalate while taking the calcium supplements (0.54 +/- 0.25 vs 0.57 +/- 0.22, p = 0.54). The effect of calcium supplements with meals, for the reduction of the risk of calcium stone formation, was unchanged, even in a population whose oxalate intake is rather low. Taking calcium supplements resulted in a reduction in urinary oxalates and an elevation in urinary citrates. Both alterations in urinary constituents counterbalanced the elevation in urinary calcium which resulted from the calcium supplements.

Adult↗
PubMed2006

[Study on irritation of calcium oxalate crystal in raw Pinellia ternata].

OBJECTIVE: Confirm the irritation of needle-like calcium oxalate crystals in raw Pinellia ternata. METHOD: Comparing the irritations of raw P. ternate containing calcium oxalate crystals, the raw P. ternate no containing calcium oxalate crystals, the pure needle-like calcium oxalate crystals isolated from raw P. ternata, the extracts of water and various solvents from raw P. ternate. by using the model of rabbits' eyes. Studying the quantity effect relationship of different concentration suspensions of needle-like calcium oxalate crystal isolated from raw P. ternate on rabbits' eyes. Observing the shape and appearance of calcium oxalate crystals in raw P. ternate and raw India Madder Root by the electro microscope and comparing their irritation degrees with the same contents of calcium oxalate crystals. RESULT: Calcium oxalate crystals in raw P. ternata showed very strong irritation property. Under the same content of calcium oxalate crystals, the irritation of raw P. ternata and pure needle-like calcium oxalate crystals isolated from raw P. ternate had no significant difference. The concentrations of needle-like calcium oxalate crystals were do relative to the degree of irritation on rabbits' eyes and they showed undoubted quantity-effect relationship. CONCLUSION: Calcium oxalate crystal is the irritation component in raw P. ternata.

Animals↗
PubMedDate not supplied

[Kinetics of oxalate in hemodialysis].

Regular dialysis treatment (RDT) does not obviate hyperoxalemia of chronic renal failure (CRF). However, there is emerging evidence suggesting that current dialysis prescription is not always associated with progressive oxalate accumulation. In view of the controversy still concerning this issue we have investigated on plasma profiles and dialysis kinetics of oxalate in patients on RDT. Oxalate was determined by ion chromatography on serum ultrafiltrates and on the whole dialysate in 23 stable patients on RDT for end-stage renal failure unrelated to primary hyperoxaluria. Nine patients were on traditional hemodialysis (HD) and 14 on soft hemodiafiltration (HDF). Plasma profiles showed that dialysis patients were virtually always hyperoxalemic. Dialysis reduced plasma oxalate by more than 60%. There was a post-dialysis oxalate rebound averaging 9.6% at 30 minutes from the end of dialysis. Oxalate dialyzer clearances were mildly higher on HDF than on HD, and were lower than both urea and creatinine clearances, irrespective of the dialysis technique. Distribution space of oxalate was 21.5 1, that is 37.3% of dry body weight, and was quite similar to estimates obtained in normal subjects and in patients with CRF by alternative isotope dilution methods. Oxalate appearance rate averaged 337 +/- 69 mumol/24 h and was not different from the daily oxalate excretion assessed in 40 healthy subjects. Oxalate appearance was significantly related to urea generation and protein catabolic rates. From our results we conclude that, unless metabolic generation of oxalate is increased, current dialysis programs should prevent progressive oxalate accumulation in the majority of the patients.

Female↗
PubMed2004

Heterologous expression of barley and wheat oxalate oxidase in an E. coli trxB gor double mutant.

Oxalate oxidase catalyses the degradation of oxalic acid to carbon dioxide and hydrogen peroxide and is of commercial importance for clinical analyses of oxalate in biological samples. Novel potential applications for oxalate oxidase include the prevention of the formation of calcium oxalate incrusts in pulp and paper manufacture and rapid determination of oxalic acid in process waters. The potential in using oxalate-degrading enzymes in industrial processes increases the interest in finding systems for heterologous expression. Oxalate oxidase from barley is a secreted multimeric glycosylated manganese-containing enzyme with several disulfide bridges, which have been found to be essential for the catalytic activity. Attempts to achieve expression of active heterologous oxalate oxidase in bacteria have up to now met little success. In this study, one oxalate-oxidase-encoding cDNA from barley and two from wheat were cloned and tested with regard to expression in Escherichia coli. The results suggest that the selection of a novel commercially available E. coli host strain, which has the ability to form disulfide bridges in heterologous proteins expressed in its cytoplasm, was important for successful expression. Although a considerable part of the heterologous protein was produced in an insoluble and inactive form, this strain, E. coli Origami B(DE3), in addition yielded soluble and active barley and wheat oxalate oxidase. One of the wheat cDNAs, Ta(M)OXO1, gave three-fold higher activity than the barley cDNA, Hv(H)OXO1, while the other wheat cDNA, Ta(M)OXO2, gave no detectable activity. This indicates that the choice of cDNA was also critical despite the high identity between the cDNAs and the encoded polypeptides (88-89% on the nucleotide level and 88-92% on the amino-acid level). Gel filtration of cell extracts containing heterologous barley and wheat oxalate oxidase resulted in an increase in the activity. This indicates that low molecular weight inhibitory compounds were present in the E. coli lysates but could be removed by the introduction of a purification step.

Amino Acid Sequence↗
PubMed2002

Structure of oxalate decarboxylase from Bacillus subtilis at 1.75 A resolution.

Oxalate decarboxylase is a manganese-dependent enzyme that catalyzes the conversion of oxalate to formate and carbon dioxide. We have determined the structure of oxalate decarboxylase from Bacillus subtilis at 1.75 A resolution in the presence of formate. The structure reveals a hexamer with 32-point symmetry in which each monomer belongs to the cupin family of proteins. Oxalate decarboxylase is further classified as a bicupin because it contains two cupin folds, possibly resulting from gene duplication. Each oxalate decarboxylase cupin domain contains one manganese binding site. Each of the oxalate decarboxylase domains is structurally similar to oxalate oxidase, which catalyzes the manganese-dependent oxidative decarboxylation of oxalate to carbon dioxide and hydrogen peroxide. Amino acid side chains in the two metal binding sites of oxalate decarboxylase and the metal binding site of oxalate oxidase are very similar. Four manganese binding residues (three histidines and one glutamate) are conserved as well as a number of hydrophobic residues. The most notable difference is the presence of Glu333 in the metal binding site of the second cupin domain of oxalate decarboxylase. We postulate that this domain is responsible for the decarboxylase activity and that Glu333 serves as a proton donor in the production of formate. Mutation of Glu333 to alanine reduces the catalytic activity by a factor of 25. The function of the other domain in oxalate decarboxylase is not yet known.

Bacillus subtilis↗
PubMed1993

Characteristics of the transport of oxalate and other ions across rabbit proximal colon.

In order to characterize oxalate handling by the P2 segment of the rabbit proximal colon, the fluxes of [14C]oxalate, 22Na+, and 36Cl- were measured in vitro using conventional short-circuiting techniques. In standard buffer the proximal colon exhibited net secretion of Na+ (-2.31 +/- 0.64 mu equiv cm-2 h-1), negligible net Cl- transport, and net secretion of oxalate (-12.7 +/- 1.6 pmol cm-2 h-1). Replacement of buffer Na+ or Cl- abolished net oxalate secretion, while HCO(3-)-free media revealed a net absorption of oxalate (19.3 +/- 4.2 pmol cm-2 h-1) and stimulated NaCl absorption. Mucosal amiloride and dimethylamiloride (1 mM) significantly reduced the unidirectional fluxes of oxalate and enhanced sodium secretion by decreasing JNams. The anion exchange inhibitor 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS; 0.1 mM, both sides) reduced the unidirectional fluxes of oxalate and chloride. Serosal epinephrine (50 microM) stimulated oxalate absorption (21.3 +/- 6.3 pmol cm-2 h-1) and sodium absorption (5.71 +/- 1.20 mu equiv cm-2 h-1), whereas dibutyryl-cAMP enhanced oxalate secretion (-43.4 +/- 6.9 pmol cm-2 h-1) and stimulated chloride secretion (-7.27 +/- 0.64 mu equiv cm-2 h-1). These results indicate that the P2 segment of the proximal colon possesses (a) secretory as well as absorptive capacities, (b) oxalate fluxes that are mediated by pathways involving Na+, Cl-, HCO3- transport and (c) a net oxalate flux that is sensitive to absorptive and secretory stimuli.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed2006

Effect of high and low calcium diets on stone forming risk during liberal oxalate intake.

PURPOSE: Recent studies suggest that a high calcium diet protects against calcium oxalate stone formation. We compared the effect of high and low calcium diets on urinary saturation of calcium oxalate during liberal oxalate intake. MATERIALS AND METHODS: A total of 10 healthy subjects (5 male, 5 female) participated in a 2-phase, randomized, crossover study comparing high (1,000 mg daily) and low (400 mg daily) calcium intake on a liberal oxalate diet (200 mg daily). During each phase subjects adhered to an instructed diet for 3 days followed by a controlled, metabolic diet for 4 days. Blood and 24-hour urine specimens collected on the last 2 days of each phase were analyzed for serum biochemistry studies and stone risk factors, respectively. RESULTS: Urinary calcium was higher (mean +/- SD 171 +/- 64 vs 124 +/- 49 mg daily, p = 0.002) and oxalate was lower (25 +/- 4.8 vs 27 +/- 4 mg daily, p = 0.02) on the high vs low calcium diet. Overall, the urinary relative saturation ratio of calcium oxalate was higher on the high compared with the low calcium diet (3.3 vs 2.5, p <0.0001) even after adjusting for confounding variables. CONCLUSIONS: In normal subjects urinary saturation of calcium oxalate was higher on a high calcium diet than a low calcium diet during liberal oxalate intake because the decrease in urinary oxalate did not overcome the effect of increased calcium. A high calcium diet during liberal oxalate intake may pose an increased risk of calcium oxalate stone formation.

Adult↗
PubMed1989

Effect of oxalate on function of kidney mitochondria.

The effects of oxalate on kidney mitochondria were evaluated in vitro to test whether oxalate exposure leads to derangement(s) in mitochondrial function that could in turn promote the formation of kidney stones. Our previous studies demonstrated that oxalate is transported across the mitochondrial membrane via the dicarboxylate carrier. The present studies indicated that oxalate competitively inhibits the uptake and oxidation of exogenous malate and succinate in isolated mitochondria but has no effect on mitochondrial respiration in the presence of a mixture of glutamate plus malate or glutamate plus pyruvate. Oxalate attenuates the increase in mitochondrial respiration produced by the uncoupler CCCP or by the Ca2+ ionophore A23187, and the latter effect is more pronounced in kidney than in liver mitochondria. The apparent Ki of oxalate for the response to Ca2+ ionophore is 1.9 +/- 0.3 mM in kidney and 6.1 +/- 0.2 mM in liver mitochondria. Similarly, the ability of oxalate to attenuate calcium-induced swelling of mitochondria is more dramatic in kidney than in liver mitochondria (apparent KiS of 1.7 +/- 0.1 and 18.2 +/- 0.7 mM, respectively). Oxalate has no effect on the rate of calcium uptake by energized mitochondria or on the rate of ruthenium red-insensitive calcium efflux from mitochondria in either tissue. The above findings indicate that oxalate interacts with the inner mitochondrial membrane or with processes controlling membrane integrity to a greater extent in kidney than liver mitochondria. The effects of oxalate on membrane permeability or integrity may be more important than its effects on mitochondrial energy production or calcium sequestration in the pathogenesis of calcium oxalate microlith formation in the kidney.

Animals↗
PubMed2001

Oxalate content of soybean seeds (Glycine max: Leguminosae), soyfoods, and other edible legumes.

Consumption of soybeans and food products made from them is increasing because of their desirable nutritional value. However, the oxalate content of seeds from 11 cultivars of soybean showed relatively high levels of total oxalate from 0.67 to 3.5 g/100 g of dry weight. Oxalate primarily was found as calcium oxalate crystals. Thirteen tested commercial soyfoods contained between 16 and 638 mg of total oxalate per serving. These values compare to those of three other legume foods, peanut butter, refried beans, and lentils, which contained 197, 193, and 100 mg of total oxalate per serving, respectively. After oxalate has been absorbed from the diet, it cannot be metabolized and is excreted by the kidney into urine, where it binds to calcium forming an insoluble salt that may precipitate to form kidney stones. The amounts of total oxalate in soybean seeds, soy foods, and other common legume foods exceed current recommendations for oxalate consumption by individuals who have a history of calcium oxalate kidney/urinary stones. This study serves as the basis to find soybean cultivars lower in oxalate, which will have lower risk for kidney stone formation after human consumption.

Calcium Oxalate↗
PubMed1990

Oxalate:OH exchange across rat renal cortical brush border membrane.

We demonstrated the presence of oxalate:OH exchange in rat renal brush border membrane. Transient concentrative uptake of oxalate ("overshoot") was observed in the presence of an inside alkaline (pH = 8.5 inside, 6.5 outside) pH gradient, but this pH gradient-stimulated oxalate uptake was abolished by 1 mM DIDS, indicating that DIDS-sensitive and -insensitive oxalate uptake mechanisms were present. The DIDS-sensitive oxalate uptake was temperature-dependent and saturable with a Km of 0.0365 mM and a Vmax of 1.38 nmol.30 second-1.mg protein-1. In addition, oxalate was transported into the osmotically active internal space. In the presence of the pH gradient, a change in transmembrane potential had no effect on pH gradient-stimulated oxalate uptake. Oxalate was exchanged for OH and this exchange was sensitive to inhibition by DIDS. Inhibition by DIDS, furosemide and probenecid facilitated the distinction of oxalate:OH exchange from formate:Cl and oxalate:Cl exchange. In preparation of our brush border membrane vesicles, no apparent SO4:HCO3 exchange was present. These data indicate that oxalate:OH exchange occurs on the brush border membrane.

Animals↗
PubMed1982

Hyperoxaluria in idiopathic calcium stone disease: further evidence of intestinal hyperabsorption of oxalate.

1. Seventeen healthy controls and 63 patients with idiopathic calcium stone disease of the urinary tract were investigated for urinary calcium and oxalate excretion and for [14C]oxalate intestinal absorption. 2. Under comparable controlled dietary intake a significant increase in calcium excretion as found in patients with stone disease. Oxalate excretion and [14C]oxalate intestinal absorption were mildly but not significantly increased. When patients with stone disease were subdivided into normocalciuric and hypercalciuric subjects, oxalate excretion and [14C]oxalate absorption were significantly increased in the latter. There was a significant direct relationship between calcium excretion and both oxalate excretion and [14C]oxalate absorption. 3. [14C]Oxalate absorption increased significantly in 22 stone-formers when dietary calcium was changed from normal to low. 4. The kinetics of [14C]oxalate intestinal absorption showed that the main difference between normocalciuric and hypercalciuric subjects occurred within the first 6 h after the oxalate-labelled meal. 5. These results confirm that mild hyperoxaluria is a frequent feature of idiopathic calcium stone disease even when patients and controls are studied under controlled dietary conditions. Our data are consistent with the hypothesis that hyperoxaluria is secondary to calcium hyperabsorption and is upper intestinal in origin.

Adult↗
PubMed1997

Effect of seed crystals of uric acid and monosodium urate on the crystallization of calcium oxalate in undiluted human urine in vitro.

1. The aim of this study was to determine whether seed crystals of uric acid or monosodium urate promote the epitaxial deposition of calcium oxalate in undiluted human urine. The effects of seed crystals of uric acid, monosodium urate or calcium oxalate on calcium oxalate crystallization induced in pooled 24-h urine samples collected from six healthy men were determined by [14C]oxalate deposition and Coulter counter particle analysis. The precipitated crystals were examined by scanning electron microscopy. 2. Seed crystals of uric acid, monosodium urate and calcium oxalate increased the precipitated particle volume in comparison with the control containing no seeds by 13.6%, 56.8% and 206.5% respectively, whereas the deposition of [14C]oxalate in these samples relative to the control was 1.4% (P < 0.05), 5.2% (P < 0.01) and 54% (P < 0.001) respectively. The crystalline particles deposited in the presence of monosodium urate seeds were smaller than those in the control samples. Scanning electron microscopy showed that large aggregates of calcium oxalate were formed in the presence of calcium oxalate seeds, which themselves were not visible. In contrast, monosodium urate and, to a lesser extent, uric acid seeds were scattered free on the membrane surfaces and attached like barnacles upon the surface of the calcium oxalate crystals. 3. It was concluded that seed crystals of monosodium urate and uric acid do not promote calcium oxalate deposition to a physiologically significant degree in urine. However, binding of monosodium urate and uric acid crystals and their subsequent enclosure within actively growing calcium oxalate crystals might occur in vivo, thereby explaining the occurrence of mixed urate/oxalate stones.

Calcium Oxalate↗
PubMed2001

The effects of oxalate-containing products on the exposed dentine surface: an SEM investigation.

In-office products containing oxalates have been claimed to be clinically effective in reducing dentine sensitivity, although there has been limited supporting clinical data. The rationale for their use appears to be based on their potential to act as occluding and/or nerve desensitizing agents. Four commercially available oxalate-containing products were applied to etched dentine discs and the extent of tubule occlusion was observed by scanning electron microscopy. Tenure Quick (aluminium oxalate), Sensodyne Sealant (ferric oxalate) and MS Coat (oxalic acid) covered the dentine surface and occluded the tubules. However, Butler Protect (potassium oxalate) did not cover the surface to any great extent but provided some occlusion. The presence of oxalates after application to glass slides and dentine discs was examined using thin film X-ray diffraction. From samples on glass, only potassium oxalate could be clearly identified (JCPDS 14-0845). No oxalate was detected on dentine discs in either thin film geometry or standard theta two theta mode. We have demonstrated that professionally applied in-office products containing oxalate are capable of covering the dentine surface and/or occluding the tubules to varying degrees. However, X-ray diffraction analysis was unable to confirm the oxalate profile for all products as described in the available commercial literature.

Acid Etching, Dental↗