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PubMed1975

An isotopic study of oxalate excretion in sheep.

Intravenously injected 14C labelled oxalate was rapidly removed from the blood stream via the kidney in 2 sheep, 75% being cleared within 8 h. Mean daily urinary oxalate excretions over 5 days were 21-2 and 27-5 mg and the derived plasma oxalate concentrations were 52-6 and 74-4 mug/100 ml, respectively. Oxalate was both filtered and secreted by the renal tubule with oxalate/inulin ratios varying from 1-11 to 1-57 in 6 normal sheep. A large increase in calcium excretion induced by calcium borogluconate infusion over 5 days was accompanied by a small but consistent increase in urinary oxalate excretion relative to calcium. Oxalate in blood was to be found mainly in the plasma, there being a small (8%) proporation within erythrocytes. This is lower than that reported for man, and yet in its excretion of oxalate via the kidney the sheep appears to closely resemble man and dog.

Animals↗
PubMed1984

Calcium oxalate kidney stones in patients on continuous ambulatory peritoneal dialysis.

Kidney stones were passed by ten out of 186 patients with endstage renal disease who were treated with continuous ambulatory peritoneal dialysis (CAPD). Stones from seven patients were examined by x-ray diffraction. In five of them the stones were composed of calcium oxalate monohydrate. The urine calcium oxalate activity product was determined in 44 CAPD patients, eight of whom were stone formers, and compared to that of 120 normal volunteers. In CAPD patients, mean urine ionic-calcium concentration was lower than in normal subjects whereas mean urine ionic-oxalate concentration was significantly higher than in normal subjects. In normal urine samples, the calcium oxalate activity product showed a significant correlation with both the urine ionic-calcium and the ionic-oxalate concentrations. In contrast, in CAPD patients the calcium oxalate activity product correlated with the ionic-calcium concentration but not with ionic-oxalate. Although the urine ionic-calcium concentration is lower in CAPD patients than in normal subjects, it is the relative increase in its concentration which appears to be associated with the increased risk of kidney stone formation in these patients. This relative hypercalciuria seems to follow 1,25(OH)2 vitamin D3 administration.

Calcitriol↗
PubMed1986

The determination of oxalate in haemodialysate and plasma: a means to detect and study 'hyperoxaluria' in haemodialysed patients.

In order to find out whether hyperoxaluria can be demonstrated in patients on chronic (twice a week) haemodialysis, a group of 13 patients was investigated. These included one patient with proven primary hyperoxaluria, one suspected of having this disease and 11 patients in whom no information was available as to their oxalate metabolism. Oxalate concentrations in haemodialysate fractions and blood samples, taken before and after dialysis, were determined. The patient with primary hyperoxaluria had a plasma oxalate concentration before dialysis above 100 mumol/l and after dialysis above 25 mumol/l, while the oxalate concentration in haemodialysate at the start of dialysis was above 25 mumol/l and at the end above 10 mumol/l. The patient suspected of hyperoxaluria had similar values. Of the remaining 11 patients, one was shown to exhibit a transient hyperoxaluria, but the others showed a normal oxalate metabolism. A plasma oxalate/creatinine concentration ratio exceeding 0.1, and the calculated total quantity of oxalate removed by dialysis exceeding 2 mmol, also enabled a diagnosis of hyperoxaluria to be made. Hyperoxaluria can still be demonstrated in patients, who because of renal failure are subjected to haemodialysis. Measurements of oxalate in haemodialysate and plasma are valuable in cases where kidney transplantations are considered, especially when the particular patient exhibits hyperoxaluria.

Adolescent↗
PubMed1993

Dissolved urate promotes calcium oxalate crystallization: epitaxy is not the cause.

1. Increasing the concentration of dissolved urate promotes the crystallization of calcium oxalate from urine. The possibility was investigated that this effect may be caused by heterogeneous nucleation of calcium oxalate by particles of crystalline urate. 2. Urine samples were collected from 10 healthy men, centrifuged and filtered, and a solution of sodium urate was added to increase the medium urate concentration from 2.2 to 5.6 mmol/l. Calcium oxalate crystallization was induced by the addition of oxalate, followed by incubation for 90 min in a shaking waterbath at 37 degrees C. The crystalline material was filtered out and the urate concentration was determined in the filtrate. 3. No difference in the urate concentration before and after induction of calcium oxalate crystallization was observed. These findings were confirmed by infra-red spectroscopy, X-ray powder diffraction and ultraviolet wet chemical analysis with detection limits of 5-10, 1.0 and 0.055%, respectively; urate was not detected in the calcium oxalate crystals. 4. In addition, three urine samples were collected and passed through 10 kDa ultrafiltration membranes to remove any colloidal particles which might have been present. The urate concentration was increased and an oxalate load was added as before, prior to incubation at 37 degrees C in a shaking water bath for 5 min, followed by passage through 10 kDa ultrafiltration membranes. Scanning electron microscopy revealed no particles on the membranes thereby indicating that colloidal or crystalline urate was not formed early in the crystallization experiments.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Tamm-Horsfall mucoprotein reduces promotion of calcium oxalate crystal aggregation induced by urate in human urine in vitro.

1. Increasing the concentration of dissolved urate promotes calcium oxalate crystallization in urine from which Tamm-Horsfall mucoprotein, an inhibitor of calcium oxalate crystal aggregation, has almost completely been removed. This study aimed to determine whether the effect of urate could be reduced or abolished by a physiological concentration of Tamm-Horsfall mucoprotein. This was approached in two ways. 2. The effect of Tamm-Horsfall mucoprotein on calcium oxalate crystallization induced by urate was tested in ultrafiltered (10 kDa) urine samples from 10 healthy men. Tamm-Horsfall mucoprotein (35 mg/l) was added to half of each specimen, the urate concentration was increased by the addition of sodium urate solution and crystallization was induced by a standard load of oxalate. The remainder of each urine specimen was used as a control; these specimens were treated with an identical amount of urate solution, but contained no Tamm-Horsfall mucoprotein. Tamm-Horsfall mucoprotein had no effect on the urinary metastable limit or on the deposition of calcium oxalate, but significantly reduced the size of the particles precipitated. 3. The effect of increasing the urate concentration in the presence of Tamm-Horsfall mucoprotein was tested. Tamm-Horsfall mucoprotein (35 mg/l) was added to 10 ultrafiltered urine samples as before, the samples were divided, and the concentration of urate was increased in half of each specimen. Compared with the control to which no urate was added, urate significantly reduced the amount of oxalate required to induce spontaneous calcium oxalate nucleation and increased the median volume and the particle size of the material deposited.(ABSTRACT TRUNCATED AT 250 WORDS)

Calcium Oxalate↗
PubMed2002

Oxalate content and calcium binding capacity of tea and herbal teas.

Thirty-two commercially available teas consisting of green, oolong and black teas were bought from supermarkets in Christchurch, New Zealand in June 2001. Fifteen herbal teas were also purchased at the same time. The soluble oxalate content of the infusate made from each of the teas was determined using high pressure liquid chromatography. The mean soluble oxalate contents of black tea in tea bags and loose tea leaves were 4.68 and 5.11 mg/g tea, respectively, while green teas and oolong tea had lower oxalate contents, ranging from 0.23 to 1.15 mg/g tea. The soluble oxalate content of the herbal teas ranged from not detected to 3.00 mg/g tea. A regular tea drinker consuming six cups of tea/day would have an intake of between 26.46 and 98.58 mg soluble oxalate/day from loose black tea, 17.88 and 93.66 mg soluble oxalate/day from black tea in tea bags and a maximum of 18.0 mg/day from herbal teas. The oxalate intake from the regular daily consumption of black teas is modest when compared to the amounts of soluble oxalate that can be found in common foods. However, oxalate in black teas has the potential to bind to a significant proportion of calcium in the milk, which is commonly consumed with the black teas.

Animals↗
PubMed1998

Peritoneal clearance and peritoneal transfer of oxalic acid, vitamin C, and vitamin B6 during continuous ambulatory peritoneal dialysis.

The peritoneal clearance and peritoneal transfer of oxalic acid, vitamin C, and vitamin B6 in 32 patients during continuous ambulatory peritoneal dialysis (CAPD) using peritoneal dialysis solutions containing 1.5% or 2.5% glucose were examined. The plasma level of oxalic acid was significantly elevated in all patients, plasma vitamin C was in the normal range or in the upper margin of the normal range, and plasma vitamin B6 was in the normal range. The peritoneal clearance of oxalic acid was significantly lower, and the peritoneal clearance of vitamin B6 was the lowest in comparison to the peritoneal clearance of urea. With the exception of vitamin B6, the peritoneal clearance and peritoneal transfer of the examined parameters increased using the dialysis solution containing 2.5% glucose. We found direct relationships between the plasma levels of oxalic acid and creatinine as well as plasma vitamin C and between the peritoneal transfer of oxalic acid and the peritoneal transfer of vitamin C as well as vitamin B6. The significant hyperoxalemia of our patients was found to persist despite the relatively high peritoneal transfer of oxalic acid during CAPD. These results suggest that CAPD is not a method effective enough for permanent reduction of the plasma levels of oxalic acid.

Adult↗
PubMed2005

Long-term, low-dose, intravenous vitamin C leads to plasma calcium oxalate supersaturation in hemodialysis patients.

BACKGROUND: Ascorbate supplementation for patients on regular dialysis treatment (RDT) is advised to obviate deficiency and improve epoetin response in those with functional iron deficiency. However, clear-cut safety concerns regarding hyperoxalemia are still poorly understood. This study tries to establish safety/efficacy profiles of ascorbate and oxalate during long-term intravenous ascorbate supplementation. METHODS: A prospective study was performed in 30 patients on RDT showing ascorbate deficiency (plasma ascorbate < 2.6 mg/L [<15 micromol/L]): 18 patients were administered intravenous ascorbate during 18 months (250 mg/wk, subsequently increased to 500 mg), and 12 patients were taken as reference untreated cases. Plasma ascorbate and oxalate assays and dialytic balance determinations were performed (ion chromatography and reverse-phase high-performance liquid chromatography, respectively) at baseline, during treatment, and 12 months after withdrawal. RESULTS: Plasma ascorbate levels increased dose dependently with supplementation (1.6 +/- 0.8 mg/L [9.1 +/- 4.6 mumol/L] at baseline, 2.8 +/- 1.8 mg/L [15.9 +/- 10.1 micromol/L]) with 250 mg of ascorbate, and 6.6 +/- 2.8 mg/L [37.5 +/- 16.0 micromol/L] with 500 mg/wk of ascorbate), but only normalized with greater dosages for several months in 94% of patients. Baseline plasma oxalate levels increased from 3.2 +/- 0.8 mg/L (35.8 +/- 8.8 micromol/L) to 3.6 +/- 0.8 mg/L (39.5 +/- 9.1 micromol/L) and 4.5 +/- 0.9 mg/L (50.3 +/- 10.4 micromol/L) with 250 and 500 mg, respectively ( P < 0.001). The calcium oxalate saturation threshold was exceeded by 7 of 18 patients (40%) during 6 months therapy with 500 mg/wk. Ascorbate dialysis removal increased from 37.8 +/- 23.2 mg (215 +/- 132 micromol) to 99.6 +/- 51.7 mg (566 +/- 294 micromol) during supplementation (P < 0.001), with corresponding increases in oxalate removal from 82.5 +/- 33.2 mg (917 +/- 369 micromol) to 111.2 +/- 32.6 mg/L (1,236 +/- 362 micromol; P < 0.01). Withdrawal reverted plasma levels and dialysis removal to initial values. Values for untreated patients did not change during 1 year of follow-up. CONCLUSION: Patients on RDT may resolve ascorbate deficiency with intravenous supplementation of 500 mg/wk, but this implies a significant risk for oxalate supersaturation. Oxalate measurements are strongly recommended during long-term ascorbate therapy.

Adult↗
PubMed2007

Acute oxalate nephropathy associated with orlistat, a gastrointestinal lipase inhibitor.

Orlistat is an oral inhibitor of gastrointestinal lipase used for weight reduction in obese patients. Although most adverse drug effects manifest in the gastrointestinal tract, this is the first reported case of orlistat-induced acute kidney injury secondary to acute oxalate nephropathy in a white woman with underlying chronic kidney disease. Acute kidney injury was associated temporally with an increased dose of orlistat and the development of increased fat malabsorption (more frequent loose oily stools). Urine sediment showed abundant calcium oxalate crystals and increased 24-hour urine oxalate concentration. Kidney biopsy showed deposition of calcium oxalate crystals within tubular lumens, consistent with acute oxalate nephropathy. Orlistat therapy was discontinued, and oral fluid intake was increased. A second kidney biopsy performed 1 month later to evaluate the slow resolution of kidney failure did not show calcium oxalate crystals within tubules. A steady improvement in renal function subsequently was observed. Results of a repeated 24-hour urine oxalate collection performed 3 weeks later when kidney function had improved were within normal limits.

Acute Disease↗
PubMed2000

Oxalate decarboxylase from Collybia velutipes. Molecular cloning and its overexpression to confer resistance to fungal infection in transgenic tobacco and tomato.

Oxalic acid is present as nutritional stress in many crop plants like Amaranth and Lathyrus. Oxalic acid has also been found to be involved in the attacking mechanism of several phytopathogenic fungi. A full-length cDNA for oxalate decarboxylase, an oxalate-catabolizing enzyme, was isolated by using 5'-rapid amplification of cDNA ends-polymerase chain reaction of a partial cDNA as cloned earlier from our laboratory (Mehta, A., and Datta, A. (1991) J. Biol. Chem. 266, 23548-23553). By screening a genomic library from Collybia velutipes with this cDNA as a probe, a genomic clone has been isolated. Sequence analyses and comparison of the genomic sequence with the cDNA sequence revealed that the cDNA is interrupted with 17 small introns. The cDNA has been successfully expressed in cytosol and vacuole of transgenic tobacco and tomato plants. The transgenic plants show normal phenotype, and the transferred trait is stably inherited to the next generation. The recombinant enzyme is partially glycosylated and shows oxalate decarboxylase activity in vitro as well as in vivo. Transgenic tobacco and tomato plants expressing oxalate decarboxylase show remarkable resistance to phytopathogenic fungus Sclerotinia sclerotiorum that utilizes oxalic acid during infestation. The result presented in the paper represents a novel approach to develop transgenic plants resistant to fungal infection.

Amino Acid Sequence↗
PubMed2003

Effect of cooking on oxalate content of pulses using an enzymatic procedure.

An enzymatic method proposed for the determination of oxalate in urine is adapted for the estimation of soluble oxalate content in beans, chickpeas and lentils. Oxalates were extracted in water by refluxing for 2 h. The method is based on the oxidation of oxalate by the oxidase and the determination of the resulting hydrogen peroxide, which in presence of peroxidase, 3-methyl-2 benzotiazinolone and 3-dimethylamino benzoic, gives an indamine compound with an absorption maximum at 590 nm. The linearity (from 0.015 to 0.6 mM) of the method is adequate to the analysis of oxalate contents in pulses, and the inter-day precision of the method expressed as relative standard deviation was good (3.01%), with an accuracy of (98.7+/-2.5%) estimated by recovery assays. This method is applied to estimate the losses of soluble oxalate as a consequence of cooking. All the cooking procedures reduce the soluble oxalate content, but microwave and industrial procedures are more effective than traditional domestic cooking.

Fabaceae↗
PubMed1993

Calcium oxalate is associated with benign breast tissue. Can we avoid biopsy?

Breast biopsies are commonly performed for abnormal, usually clustered, calcifications detected by mammography. Calcium phosphate is the predominant form of calcium seen in breast tissue and is frequently associated with malignancy. Calcium oxalate, which can also be present in breast tissue, has been exclusively associated with benign lesions. Thus, if mammography could distinguish calcium phosphate from calcium oxalate, biopsy could be avoided in some patients. Pathologic findings and corresponding mammograms of 55 patients who underwent biopsy for abnormal calcifications were reviewed. The authors evaluated such pathologic features as type of calcification, anatomic location, and association with fibrocystic changes or carcinoma. Mammographically, calcifications were categorized by size, distribution, and morphology, and each was assigned a density rating of low, medium, or high. Of the 55 cases, 41 contained calcium phosphate only, 8 contained calcium oxalate only, and 6 contained both. If only calcium oxalate was present, the calcium was always associated with benign epithelium. Of 47 cases, calcium phosphate was associated with benign breast disease in 28 and with carcinoma in 19. Five of six cases with both calcium phosphate and calcium oxalate contained carcinoma; calcium phosphate was seen in the carcinoma area in all five. Radiologically, calcium phosphate was typically medium to high density, whereas calcium oxalate was characterized as amorphous, low to medium density. Other low-density calcifications were almost always benign, unless pleomorphic in shape. Although further work is necessary to confirm these findings, it appears that, radiologically, low-density, amorphous, calcifications, even if clustered, are associated with benign breast disease, and may represent calcium oxalate. Patients with such calcifications may be managed conservatively.

Adult↗
PubMed1990

Oxalate crystal deposits in the heart in chronic renal failure: an experimental study.

The present study was undertaken to evaluate three factors which may contribute to the myocardial deposition of calcium oxalate in 5/6 nephrectomised rats: (1) increased plasma oxalate, (2) elevated plasma ionised calcium, and (3) local myocardial tissue damage. A simple increase in plasma oxalate concentrations produced by injection of sodium oxalate did not cause deposits in the heart. Increased plasma ionised calcium combined with elevated plasma oxalate for 60 days was likewise unimportant with regard to cardiac deposits. However, when local tissue damage was added by heterotopic cardiac transplantation, deposition of crystals was seen in four or five allografts damaged by rejection. In this model the rat's own heart was not affected. Although an increase in plasma oxalate values is not without significance, the present findings suggest that local tissue damage is a more important factor in the myocardial deposition of oxalate crystals in renal failure.

Animals↗
PubMed1991

Comparison of patients with idiopathic calcium phosphate and calcium oxalate stones.

Our primary objective was to test the hypothesis that a defect in acidification is more common in patients who have idiopathic calcium phosphate kidney stones than in those whose stones are formed mainly of calcium oxalate. Additionally, other risk factors might differ for these 2 stone types. Urine pH was measured serially over 24 hours, and along with ammonium and titratable acid, it was measured before and serially after ingestion of ammonium chloride in 3 groups of subjects: 24 patients with predominantly calcium phosphate stones, 30 patients with calcium oxalate stones, and 15 health non-stone-formers. Twenty-six parameters potentially related to stone formation and acidification were assayed on urines collected over 24 hours, and 15 parameters on blood. The data base was a computerized list of 5900 analyses of stones from patients living in Newfoundland. Patients not known by their physician to have had urinary tract infection, anatomical abnormality, hyperparathyroidism, or renal tubular acidosis were asked to participate in the study. Differences between means were considered significant if p values were less than 0.05 for F by analysis of variance and also less than 0.01 by t-test. In all patients with calcium oxalate stones and all non-stone-formers, urine acidified to pH less than 5.25, but in 8 of the 23 phosphate stone formers who completed the ammonium chloride study urine failed to acidify to pH less than 5.25. As all 8 had normal values for venous pH, total CO2, and chloride, they were considered to have incomplete renal tubular acidosis (IRTA). The 8 phosphate stone formers with IRTA had greater mean values for urine pH on all 9 specimens collected serially over 24 hours (all means greater than 6.2), and after administration of ammonium chloride (p less than 0.01), as well as lower mean values for urine titratable acid excretion (p less than 0.01), both after administration of ammonium chloride and in 24-hour urine samples, compared with the remaining phosphate stone formers whose urine acidified and the oxalate and non-stone-forming control groups. Nearly all the phosphate stone formers had 1 or more risk factors for stone formation, but with frequencies not significantly higher than those found in the oxalate group. Hypercalciuria and hypocitruria were the commonest, but increased oxalate or urate also occurred. Thus, idiopathic calcium phosphate stone formation can be associated with 1 or more of several risk factors, and, with the possible exception of those with IRTA, treatment should be similar to that given to patients with calcium oxalate stones.

Acidosis, Renal Tubular↗
PubMed2005

Enhancing resistance to Sclerotinia minor in peanut by expressing a barley oxalate oxidase gene.

Sclerotinia minor Jagger is the causal agent of Sclerotinia blight, a highly destructive disease of peanut (Arachis hypogaea). Based on evidence that oxalic acid is involved in the pathogenicity of many Sclerotinia species, our objectives were to recover transgenic peanut plants expressing an oxalic acid-degrading oxalate oxidase and to evaluate them for increased resistance to S. minor. Transformed plants were regenerated from embryogenic cultures of three Virginia peanut cultivars (Wilson, Perry, and NC-7). A colorimetric enzyme assay was used to screen for oxalate oxidase activity in leaf tissue. Candidate plants with a range of expression levels were chosen for further analysis. Integration of the transgene was confirmed by Southern-blot analysis, and gene expression was demonstrated in transformants by northern-blot analysis. A sensitive fluorescent enzyme assay was used to quantify expression levels for comparison to the colorimetric protocol. A detached leaflet assay tested whether transgene expression could limit lesion size resulting from direct application of oxalic acid. Lesion size was significantly reduced in transgenic plants compared to nontransformed controls (65%-89% reduction at high oxalic acid concentrations). A second bioassay examined lesion size after inoculation of leaflets with S. minor mycelia. Lesion size was reduced by 75% to 97% in transformed plants, providing evidence that oxalate oxidase can confer enhanced resistance to Sclerotinia blight in peanut.

Arachis↗
PubMed2000

Oxalic acid, a pathogenicity factor for Sclerotinia sclerotiorum, suppresses the oxidative burst of the host plant.

Effective pathogenesis by the fungus Sclerotinia sclerotiorum requires the secretion of oxalic acid. Studies were conducted to determine whether oxalate aids pathogen compatibility by modulating the oxidative burst of the host plant. Inoculation of tobacco leaves with an oxalate-deficient nonpathogenic mutant of S. sclerotiorum induced measurable oxidant biosynthesis, but inoculation with an oxalate-secreting strain did not. Oxalate inhibited production of H(2)O(2) in tobacco and soybean cultured cell lines with a median inhibitory concentration of approximately 4 to 5 mM, a concentration less than that measured in preparations of the virulent fungus. Several observations also indicate that the inhibitory effects of oxalate are largely independent of both its acidity and its affinity for Ca(2)+. These and other data demonstrate that oxalate may inhibit a signaling step positioned upstream of oxidase assembly/activation but downstream of Ca(2)+ fluxes into the plant cell cytosol.

Ascomycota↗
PubMed1981

Determination of oxalic acid clearance and plasma concentration by radioisotope infusion. Results in a family with hyperoxaluria.

The renal clearance of 14C-oxalate was studied in a family with two children suffering from primary hyperoxaluria. The 14C-oxalate/creatinine clearance ratio ranged from 1.8 to 2.6 (mean 2.0) and appeared to be independent of the glomerular filtration rate. The calculated plasma oxalate concentrations in the three normo-oxaluric subjects ranged from 0.1 to 0.9 mumol/l, whereas values of 3.2 and 16.3 mumul/l were found in the two hyperoxaluric subjects. In the latter patient, the oxalate production decreased and the clearance increased after vitamin B6 treatment, resulting in a drop in the oxalate plasma level to 5.3 mumol/l. The apparent distribution volumes, expressed as percentage of body weight, ranged from 30 to 47% (mean 35). The mean biological half-life of 14C-oxalate was 2.7 hours in the subjects with normal renal function and increased with impairment of renal function. The recovery of 14C in the urine ranged from 87 to 112% (mean 101); all 14C activity was recovered as oxalate.

Adolescent↗
PubMed2004

The role of glycoproteins in calcium oxalate crystal development.

OBJECTIVE: To assess the effects of a glycoprotein (mucine) on calcium oxalate crystal development in different conditions and situations, to clarify some of its possible effects. MATERIALS AND METHODS: Crystallization was assessed using a batch system in presence of mucine suspensions, by kinetic-turbidimetric measurements, and using a flow system in the presence of retained agglomerates of mucine, evaluating the precipitated calcium oxalate. RESULTS: In batch conditions low mucine concentrations (<15 mg/L) inhibited calcium oxalate nucleation and higher concentrations (<250 mg/L) inhibited calcium phosphate nucleation, whereas at high concentrations there was also promotion. The presence of an aggregate of mucine in the flow system provoked calcium oxalate monohydrate crystallization at 0.691 microg/h per mg of mucine. In flow conditions pyrophosphate at 11.5 micromol/L caused a decrease of 84% in the calcium oxalate crystallized on mucine, 1.32 mmol/L of citrate a decrease of a 83%, 20 mg/L of pentosan polysulphate a decrease by 80%, and 7.58 micromol/L phytate totally prevented the crystallization of calcium oxalate on mucine. CONCLUSION: All substances inhibiting calcium oxalate crystallization with the capacity to interact with calcium ions also have crystallization promoting properties when they are at sufficiently high concentrations, because of their capacity to form agglomerates or the insolubility of their calcium salts.

Calcium Oxalate↗