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PubMed2004

Dependence of oxalate absorption on the daily calcium intake.

Two to 20% of ingested oxalate is absorbed in the gastrointestinal tract of healthy humans with a daily 800 mg calcium intake. Calcium is the most potent modifier of the oxalate absorption. Although this has been found repeatedly, the exact correlation between calcium intake and oxalate absorption has not been assessed to date. Investigated was oxalate absorption in healthy volunteers applying 0.37 mmol of the soluble salt sodium [(13)C(2)]oxalate in the calcium intake range from 5 mmol (200 mg) calcium to 45 mmol (1800 mg) calcium. Within the range of 200 to 1200 mg calcium per day, oxalate absorption depended linearly on the calcium intake. With 200 mg calcium per day, the mean absorption (+/- SD) was 17% +/- 8.3%; with 1200 mg calcium per day, the mean absorption was 2.6% +/- 1.5%. Within this range, reduction of the calcium supply by 70 mg increased the oxalate absorption by 1% and vice versa. Calcium addition beyond 1200 mg/d reduced the oxalate absorption only one-tenth as effectively. With 1800 mg calcium per day, the mean absorption was 1.7% +/- 0.9%. The findings may explain why a low-calcium diet increases the risk of calcium oxalate stone formation.

Absorption↗
PubMed2005

Effects of urinary prothrombin fragment 1 in the formation of calcium oxalate calculus.

PURPOSE: We investigated the effects of urinary prothrombin fragment 1 in the formation of calcium oxalate urolithiasis. MATERIALS AND METHODS: Fresh urine and renal parenchyma from patients with calcium oxalate calculus and normal controls were collected. Urinary prothrombin fragment 1 was isolated and purified from urine. It was identified by sodium dodecyl sulfide-polyacrylamide gel electrophoresis and analysis of its first 13 N-amino acids. The inhibitory activity of urinary prothrombin fragment 1 on calcium oxalate crystal growth was tested by the seeded crystallization technique. Meanwhile, the gamma-carboxyglutamic acid composition of urinary prothrombin fragment 1 was analyzed by a previously described method and genetic mutation of the gamma-carboxyglutamic acid domain of urinary prothrombin fragment 1 from renal parenchyma was detected by polymerase chain reaction-single strand conformational polymorphism sequencing. RESULTS: The gamma-carboxyglutamic acid composition of urinary prothrombin fragment 1 was significantly decreased from normal (24.4 to 1.7 mol/1,000 amino acids) in patients with calcium oxalate calculus. The mean growth index +/- SD of urinary prothrombin fragment 1 to calcium oxalate crystals was 42.3 +/- 4.2 compared with the normal index of 19.2 +/- 2.8 (p <0.01). The polymerase chain reaction-single strand conformational polymorphism sequencing technique revealed no genetic mutation of the gamma-carboxyglutamic acid domain of urinary prothrombin fragment 1 in patients with calcium oxalate calculus. CONCLUSIONS: The gamma-carboxyglutamic acid composition of urinary prothrombin fragment 1 as well as its ability to inhibit calcium oxalate crystal growth was significantly decreased in patients with calcium oxalate calculus. This was not caused by genetic mutation of the gamma-carboxyglutamic acid domain of urinary prothrombin fragment 1. It is important to elucidate the mechanisms of calcium oxalate stones in view of urinary prothrombin fragment 1.

1-Carboxyglutamic Acid↗
PubMed2005

Vitamin E therapy prevents hyperoxaluria-induced calcium oxalate crystal deposition in the kidney by improving renal tissue antioxidant status.

OBJECTIVE: To determine whether vitamin E prevents hyperoxaluria-induced stone formation, using a new animal model of calcium oxalate stone disease, as our previous in- vitro and in-vivo studies showed that oxalate and hyperoxaluria induce free-radical generation, which results in peroxidative injury to renal tubular cells. MATERIALS AND METHODS: Ethylene glycol (EG) was administered at 150 mg/day by gavage for 3 weeks to rats fed on diets with adequate (group 1), excess (group 2) or deficient (group 3) vitamin E. Several indicators of peroxidation, free radicals and enzymatic activity were then assessed. RESULTS: EG treatment in group 1 lead to increased lipid peroxidation, protein thiol, excretion of urinary enzymes, oxalate and decreases in urinary calcium, antioxidant enzymes and altered glutathione redox balance. Although renal function was not altered, there was increased water intake, urine volume and lowered urinary pH in these rats. These changes were more intense, with extensive calcium-oxalate crystal deposition, in rats in group 3, and prevented in rats in group 2, except for urinary oxalate levels, which remained high. Histopathological examination showed that there was no deposition of calcium oxalate crystals in rats in group 2. CONCLUSION: This is the first study to demonstrate in-vivo evidence that hyperoxaluria-induced peroxidative injury induces individual calcium oxalate crystal attachment in the renal tubules. In addition, excess vitamin E completely prevented calcium oxalate deposition, by preventing peroxidative injury and restoring renal tissue antioxidants and glutathione redox balance. Therefore, vitamin E therapy might provide protection against the deposition of calcium oxalate stones in the kidney of humans.

Animals↗
PubMed1978

Studies on calcium uptake by myometrial microsomes with particular reference to the dependence on inorganic phosphate and oxalate.

Ca uptake by microsomes isolated from non-pregnant rabbit myometrium was potentiated by both inorganic phosphate (Pi) and oxalate anions. Both Pi and oxalate had little effect on the initial rate of uptake but a pronounced effect on the capacity of Ca uptake measured after 20 min which was greater in the presence of oxalate than that of Pi (5 mM each). The presence or absence of sucrose in the uptake medium had a significant effect on oxalate-induced potentiation of Ca uptake but not on that potentiated by Pi or that measured in the absence of either potentiating anion. A part of Ca accumulated additionally under the influence of sucrose could be removed by washing microsomes with KCl. Another significant difference between the pontentiating effect of oxalate and Pi was observed when the pH of the incubation medium was varied. In the presence of oxalate the pH optimum was between 6.4--6.8, whereas that in its absence or in the presence of Pi the optimal pH was around 7.2. Reduction in pH from 7.2 to 6.8 along with the substitution of KCl by sucrose resulted in 3-fold increase in Ca uptake when oxalate was used as the potentiating anion. The results suggest that Ca is taken up by a different mechanism in the presence of oxalate than that in its absence or when oxalate anion is substituted with inorganic phosphate.

Animals↗
PubMed1980

Isolation and some characteristics of anaerobic oxalate-degrading bacteria from the rumen.

Obligately anaerobic oxalate-degrading bacteria were isolated from an enriched population of rumen bacteria in an oxalate-containing medium that had been depleted of other readily metabolized substrates. These organisms, which are the first reported anaerobic oxalate degraders isolated from the rumen, were gram negative, nonmotile rods. They grew in a medium containing sodium oxalate, yeast extract, cysteine, and minerals. The only substrate that supported growth was oxalate. Growth was directly related to the concentration of oxalate in the medium (1 to 111 mM), and cell yields were approximately 1.1 g (dry weight)/mol of oxalate degraded. Oxalate was stoichiometrically degraded to CO2 and formate. These anaerobes occupy a unique ecological niche and are distinct from any previously described oxalate-degrading bacteria.

Animals↗
PubMed1997

Effect of mineral water containing calcium and magnesium on calcium oxalate urolithiasis risk factors.

Calcium oxalate kidney stone formers are invariably advised to increase their fluid intake. In addition, magnesium therapy is often administered. Recently, a prospective study showed that a high dietary intake of calcium reduces the risk of symptomatic kidney stones. The present study was performed to test whether simultaneous delivery of these factors--high fluid intake, magnesium ingestion and increased dietary calcium--could reduce the risk of calcium oxalate kidney stone formation. A French mineral water, containing calcium and magnesium (202 and 36 ppm, respectively) was selected as the dietary vehicle. Twenty calcium oxalate stone-forming patients of each sex as well as 20 healthy volunteers of each sex participated in the study. Each subject provided a 24-hour urine collection after ingestion of mineral water over a period of 3 days; after a suitable rest period the protocol was repeated using local tap water (Ca: 13 ppm, Mg: 1 ppm). In addition, 24-hour urines were collected by each subject on their free diets. The entire cycle was repeated at least twice by each subject. Several risk factors (excretion of oxalate; relative supersaturations of calcium oxalate, brushite and uric acid; calcium oxalate metastable limit; oxalate:magnesium ratio and oxalate:metastable limit ratio) were favourably altered by the mineral water and tap water regimens but the former was more effective. In addition, the mineral water protocol produced favourable but unique changes in the excretion of citrate and magnesium as well as in the relative supersaturation of brushite which were not achieved by the tap water regimen. To the contrary, tap water produced an unfavourable change in the magnesium excretion. The group which benefitted most were male stone formers in whom 9 risk factors were favourably altered by the mineral water protocol. It is concluded that mineral water containing calcium and magnesium, such as that used in this study, deserves to be considered as a possible therapeutic or prophylactic agent in calcium oxalate kidney stone disease.

Adult↗
PubMed1980

Anatomical distribution of exogenous 14C-oxalate in the rat by macroautoradiography.

A single dose of 14C-oxalate was given to a group of laboratory rats using a gastric tube. The animals were then killed at intervals of 1/2, 2, 5, 24 and 72 h following oxalate administration and the oxalate distribution was determined using the technique of macroautoradiography. The results showed that a large proportion of the absorbed oxalate was already excreted in the bladder 30 min after administration. The non-absorbed oxalate was found eliminated with the faeces after 24 h. At the same time, 14C-oxalate was demonstrated in the bones; whereas 72 h later no radioactivity could be found anymore. It is conceivable, therefore, that the rapid renal excretion of exogenous oxalate may lead to a short-term oxalate peak in the urine. More importantly, the occurrence of such a urinary oxalate peak could in turn be responsible for crystalluria and stone formation.

Animals↗
PubMed2004

Effects of oxalate on IMCD cells: a line of mouse inner medullary collecting duct cells.

Oxalate, a metabolic end product and a major constituent of the majority of renal stones, has been shown to be toxic to renal epithelial cells of cortical origin. However, it is unknown whether inner medullary collecting duct (IMCD) cells that are physiologically exposed to higher concentrations of oxalate also behave in a similar manner. In the present study, we examined the effects of oxalate on IMCD cells. IMCD cells from the mouse were maintained in DMEM/F12 media supplemented with fetal bovine serum and antibiotics. Exposure of IMCD cells to oxalate produced time- and concentration-dependent changes in the light microscopic appearance of the cells. Long-term exposure to oxalate resulted in alterations in cell viability, with net cell loss after exposure to concentrations of 2 mM or greater. The production of free radicals was directly related to the exposure time and the concentration of oxalate. Crystal formation occurred in less than 1 h and cells in proximity to crystals would lose membrane integrity. Compared with IMCD cells, LLC-PK1 cells as well as HK-2 cells showed significant toxicity starting at lower oxalate concentrations (0.4 mM or greater). These results provide the first direct demonstration of toxic effects of oxalate in IMCD cells, a line of renal epithelial cells of the inner medullary collecting duct, and suggest that the cells lining the collecting duct are relatively resistant to oxalate toxicity.

Animals↗
PubMed2006

Quantification of urinary oxalate by liquid chromatography-tandem mass spectrometry with online weak anion exchange chromatography.

BACKGROUND: Urinary oxalate is commonly measured with an enzymatic assay that is specific but requires a manual clean-up step to reduce ascorbic acid interference. We developed a urinary oxalate assay that uses liquid chromatography-tandem mass spectrometry (LC-MS/MS) with anion exchange chromatography and simple sample preparation. METHODS: We added calibrator or urine sample (10 microL) to 10 microL of (13)C2 oxalate and 400 microL of water and performed separation on a Waters OASIS WAX column, flow rate 0.6 mL/min, and then elution for 0.3 min with water containing 2 mmol/L ammonium acetate and 1 mL/L formic acid and for 1.0 min with 750 mL/L methanol containing 20 mL/L ammonia. We detected multiple reaction monitoring transitions m/z 88.6 > 60.5 and m/z 90.5 > 61.5 for oxalic acid and 13C2-oxalate, respectively, with a Quattro micro tandem mass spectrometer in electrospray-negative mode. RESULTS: Oxalate and 13C2-oxalate eluted at 1.2 min. Mean recovery was 95%, limit of detection 3.0 micromol/L, lower limit of quantification 100.0 micromol/L, linearity to 2212 micromol/L, imprecision <6%, and bias <3% at 166, 880, and 1720 micromol/L. Oxalate eluted after the main area of ion suppression. Mean response ratios for urine and aqueous samples, enriched at 200 and 1000 micromol/L, were 3.7% and 5.4%, respectively. No interference was observed from other organic acids. Passing and Bablock regression analysis comparing the Trinity Biotech enzymatic reagent set and LC-MS/MS showed LC-MS/MS = 1.06 (enzymatic assay) -21.2, r = 0.964, n = 110. Bland Altman analysis showed general agreement, with a mean bias of -1.9 mumol/L. CONCLUSION: This LC-MS/MS assay is applicable for quantifying urinary oxalate excretion.

Anion Exchange Resins↗
PubMed1998

The effect of ascorbic acid ingestion on the biochemical and physicochemical risk factors associated with calcium oxalate kidney stone formation.

The present study was undertaken to determine the effect of ingestion of large doses of vitamin C on urinary oxalate excretion and on a number of other biochemical and physicochemical risk factors associated with calcium oxalate urolithiasis. A further objective was to determine urinary ascorbate excretion and to relate it qualitatively to ingested levels of the vitamin and oxalate excretion. Ten healthy males participated in a protocol in which 4 g ascorbic acid was ingested for 5 days. Urines (24 h) were collected prior to, during and after the protocol. The urine collection procedure was designed to allow for the analysis of oxalate in the presence and absence of an EDTA preservative and for the analysis of ascorbic acid by manual titration using 2,6 dichlorophenolindophenol. Physicochemical risk factors such as the calcium oxalate relative supersaturation and Tiselius risk index were calculated from urine composition. The results showed that erroneously high analytical oxalate levels occur in the asence of preservative. In the preserved samples there was no significant increase in oxalate excretion at any stage of the protocol. Ascorbate excretion increased when vitamin C ingestion commenced but levelled out after 24 hours suggesting that saturation of the metabolic pool is reached within 24 hours after which ingested ascorbic acid is excreted unmetabolized in the urine. While transient statistically significant changes occurred in some of the biochemical risk factors, they were not regarded as being clinically significant. There were no changes in either the calcium oxalate relative supersaturation or Tiselius risk index. It is concluded that ingestion of large doses of ascorbic acid does not affect the principal risk factors associated with calcium oxalate kidney stone formation.

2,6-Dichloroindophenol↗
PubMed2006

Inhibitory effect of oxalic acid on bacterial spoilage of raw chilled chicken.

Oxalic acid was evaluated as a treatment for reducing populations of naturally occurring microorganisms on raw chicken. Raw chicken breasts were dipped in solutions of oxalic acid (0, 0.5, 1.0, 1.5, and 2.0%, wt/vol) for 10, 20, and 30 min, individually packed in oxygen-permeable polyethylene bags, and stored at 4 degrees C. Total plate counts of aerobic bacteria and populations of Pseudomonas spp. and Enterobacteriaceae on breasts were determined before treatment and after storage for 1, 3, 7, 10, and 14 days. The pH and Hunter L, a, and b values of the breast surface were measured. Total plate counts were ca. 1.5 and 4.0 log CFU/g higher on untreated chicken breasts after storage for 7 and 14 days, respectively, than on breasts treated with 0.5% oxalic acid, regardless of dip time. Differences in counts on chicken breasts treated with water and 1.0 to 2.0% of oxalic acid were greater. Populations of Pseudomonas spp. on chicken breasts treated with 0.5 to 2.0% oxalic acid and stored at 4 degrees C for 1 day were less than 2 log CFU/g (detection limit), compared with 5.14 log CFU/g on untreated breasts. Pseudomonas grew on chicken breasts treated with 0.5% oxalic acid to reach counts not exceeding 3.88 log CFU/g after storage for 14 days. Counts on untreated chicken exceeded 8.83 log CFU/g at 14 days. Treatment with oxalic acid caused similar reductions in Enterobacteriaceae counts. Kocuria rhizophila was the predominant bacterium isolated from treated chicken. Other common bacteria included Escherichia coli and Empedobacter brevis. Treatment with oxalic acid caused a slight darkening in color (decreased Hunter L value), retention of redness (increased Hunter a value), and increase in yellowness (increased Hunter b value). Oxalic acid has potential for use as a sanitizer to reduce populations of spoilage microorganisms naturally occurring on raw chicken, thereby extending chicken shelf life.

Animals↗
PubMed1999

Expression of bikunin mRNA in renal epithelial cells after oxalate exposure.

PURPOSE: To determine the changes in expression of bikunin in renal epithelial cells on exposure to oxalate and calcium oxalate crystals. MATERIALS AND METHODS: This study used reverse transcription polymerase chain reaction (RT-PCR) to examine bikunin mRNA expression levels in MDCK cells exposed to oxalate or calcium oxalate crystals. Poly(A)+ RNA was isolated directly from renal epithelial cells, then converted to cDNA with random primers and reverse transcriptase. To quantify the expression level ofbikunin mRNA, we developed a competitive DNA template for competitive PCR analysis. The PCR products were resolved by electrophoresis on 1.3% agarose gel and visualized with ethidium bromide. In this system, we could quantify the exact number of bikunin mRNA transcripts. Bikunin mRNA from rat liver was expressed as a positive control. RESULTS: Bikunin mRNAs and competitive templates from renal epithelial cells were expressed in all samples as 434 bp and 312 bp bands, respectively. Bikunin expression was significantly increased in oxalate exposed cells. Cells exposed to calcium oxalate monohydrate crystals or latex beads showed no significant change in expression of bikunin. Western blotting analysis also showed increased expression of bikunin and inter-alpha-inhibitor-related proteins in the culture medium of oxalate exposed cells. CONCLUSIONS: These findings suggest that renal epithelial cells express bikunin gene and have the capability to produce bikunin when stimulated by certain agents such as oxalate. This increased expression and production of bikunin may represent a protective response of renal epithelial cells to nephrotoxic challenges of oxalate.

Animals↗
PubMed2000

Calcium oxalate and iron accumulation in sarcoidosis.

BACKGROUND: In many patients with sarcoidosis, the granulomas contain inclusion bodies within giant cells. Many giant cells contain crystalline oxalate that chemically coordinates iron on the surface of the crystal. If this iron is incompletely coordinated and capable of redox cycling, then oxalate might contribute to granuloma formation in the lung. METHODS: Using human tissues, isolated alveolar macrophages and respiratory epithelial cells, we measured the ability of calcium oxalate to sequester iron, stimulate cytokine release and cause granuloma formation. We then studied the effects of in vivo oxalate instillation on pulmonary granuloma formation over 3 to 6 months in rats. RESULTS: Calcium oxalate present in human sarcoid granulomas sequesters significant amounts of iron and ferritin. In alveolar macrophage cultures, oxalate accumulates iron and stimulates ferritin production and giant cell formation. In cultured respiratory epithelial cells, calcium oxalate increases the release of two interleukins (IL), IL-8 and IL-6, involved in granuloma formation by 8 to 10 fold within 24 hours. Intratracheal instillation of calcium oxalate crystals into the lungs of rats is associated with pulmonary iron and ferritin accumulation and organic carbonyl formation consistent with sustained oxidative stress. These exposures were accompanied by influx of alveolar macrophages, giant cell formation, and a granulomatous response in the lung. CONCLUSIONS: These results support an association between calcium oxalate deposition in the lung, iron mediated oxidative stress and formation of some of the granulomas of sarcoidosis.

Adolescent↗
PubMed2001

The use of oxalate to reduce dentin permeability under adhesive restorations.

PURPOSE: To test a novel approach to reducing dentin permeability that localizes occlusion of dentin tubules by calcium oxalate crystals to the subsurface without lowering resin bond strengths to oxalate-treated dentin surfaces. MATERIALS AND METHODS: Flat dentin surfaces of extracted human third molars were etched with a mass fraction of 32% phosphoric acid (Bisco) for 15 s and rinsed. Half of the surface was treated with a potassium oxalate gel (mass fraction of 3% monopotassium monohydrogen oxalate) for 2 mins. The entire surface was then moist bonded with either One Step (OS) or Scotchbond Multi-Purpose (SB) adhesive systems. A resin-based composite (Z-100) buildup was made over the entire surface. After storage for 24 hrs in distilled water, the teeth were longitudinally sectioned to separate the oxalate-treated half from the untreated (control) half. Each half was serially sectioned into several 0.7 mm thick slabs which were then trimmed to an hour-glass shape to reduce the bonded area to approximately 0.8 mm2 and tested in tension. Pre- and post-treatment hydraulic conductance (Lp) of dentin was determined using dentin discs with a standard protocol. SEM images were obtained to examine the effects of treatment both on the dentin surface and along the tubules beneath the surface. The bonded interface was also examined by SEM. RESULTS: Treating etched dentin discs with the oxalate gel caused significant reduction of the Lp of dentin (80% reduction, P < 0.05). There were no statistically significant differences between bond strengths of oxalate-treated and untreated surfaces for either adhesive system. OS resulted in a bond strength of 25.8 +/- 9.2 MPa to untreated and 27.8 +/- 8.9 MPa to oxalate treated surfaces (P > 0.05). SB showed bond strengths of 22.9 +/- 7.9 MPa and 22.9 +/- 9.6 MPa to untreated and treated surfaces, respectively (P > 0.05). SEM images showed that the application of potassium oxalate gel on etched dentin resulted in the formation of crystals inside the tubules rather than on the surface. Examination of the bonded interfaces demonstrated that the crystal formation inside the tubules did not compromise the formation of a typical hybrid layer on the top of dentin surfaces. Resin monomers penetrated into the tubules filling the spaces around the crystals forming resin tags with a jagged-like feature.

Analysis of Variance↗
PubMed2002

Effects of oxalate on HK-2 cells, a line of proximal tubular epithelial cells from normal human kidney.

PURPOSE: Oxalate, a metabolic end product, is a major constituent of majority of renal stones. Previous studies with LLC-PK1 cells, a line of proximal renal epithelial cells of porcine origin, have shown that oxalate produces time and concentration dependent effects on the growth and viability of these cells. We assessed the possibility that oxalate may be toxic to HK-2 cells, a line of human proximal renal epithelial cells. MATERIALS AND METHODS: HK-2 cells were maintained in Dulbecco's modified Eagle's medium supplemented with fetal bovine serum and antibiotics. Cells were exposed to oxalate for various intervals. Trypan blue exclusion criteria were used to assess membrane integrity, cell morphology was assessed by hematoxylin and eosin staining and crystal violet staining was used to measure cell density. DNA synthesis was measured by [3H]-thymidine incorporation and superoxide production was measured by the nitroblue tetrazolium reduction method. RESULTS: Exposure of HK-2 cells to oxalate produced time and concentration dependent increase in the membrane permeability to trypan blue and changes in the light microscopic appearance of the cells. Long-term exposure to oxalate resulted in an increase in DNA synthesis and alterations in cell viability with net cell loss after exposure to high oxalate concentrations. CONCLUSIONS: To our knowledge the results provide the first direct demonstration of the toxic effects of oxalate in HK-2 cells, a line of human renal epithelial cells, and suggest that hyperoxaluria may contribute to renal tubular damage associated with calcium oxalate stone disease.

Cell Division↗
PubMed2004

[Difference in oxalate content between buckwheat and soybean leaves and its possible cause].

Buckwheat (Fagopyrum esculentum M.) and soybean (Glycine max L.) seedlings with expanded primary leaves were grown in 1/5 Hoagland culture solution for 10 d, then oxalate content was determined in leaves, roots and root exudates. The result showed that its content in buckwheat was much higher than that in soybean, respectively. This clearly indicated that the oxalate content difference in the leaves was due to the metabolic difference rather than to the different rate in transport to the roots and/or in exudation. Activity of oxalate-degrading enzyme oxalate oxidase could be detected in buckwheat, but not in soybean leaves, implicating that buckwheat leaves had some oxalate-degrading capability. This further demonstrated that the oxalate difference was caused by the change in the oxalate biosynthetic process. Buckwheat leaves contained more glyoxylate, and also higher glyoxylate-oxidizing activity of glycolate oxidase (GO) than soybean. GO from buckwheat had a lower Km for glyoxylate than that from soybean. In combination with the higher level of glyoxylate, buckwheat leaves might have higher rate of oxalate formation from glyoxylate. It is suggested that the rate of glyoxylate oxidation by GO may be one of the critical steps which control oxalate accumulation in plants.

Alcohol Oxidoreductases↗
PubMed2005

[Influence of urinary citrate levels on spontaneous calcium oxalate dihydrate crystalluria].

INTRODUCTION: Calcium oxalate is the leading cause of renal stones and is mainly due to hypercalciuria, hyperoxaluria and/or hypocitraturia. Citrate is considered to be an effective inhibitor of calcium oxalate crystallization and is therefore increasingly prescribed as maintenance therapy for patients with calcium stones, but no study has investigated the effect of urinary citrate levels on spontaneous calcium oxalate crystalluria in human urine. In this study, the authors examined the relationships between the calcium oxalate molar product, the urinary citrate concentration and weddellite (oxalate calcium dihydrate) crystalluria, the most frequent crystalline form of calcium oxalate in human urine. MATERIAL AND METHODS: Crystalluria analysis and calcium, oxalate and citrate assays were performed on a series of 10,222 first morning urine samples from 4,809 stone patients and 453 first morning urine samples from 317 control subjects. The frequency and characteristics of weddellite crystalluria were determined as a function of the calcium oxalate molar product (pCaOx) and urinary citrate concentration. RESULTS: 1,940 urine samples (18.2%) presented weddellite crystalluria, which was pure in 1,378 urine samples from stone patients (13.5%) and 43 urine samples (9.5%) from controls (p < 0.05). The crystalluria rate in stone patients ranged from 4% for pCaOx < 1 (mmol/l)2 to 81.3% for pCaOx > or = 3 (mmol/l)2 (p < 0.0001). Over the same interval of pCaOx, weddellite crystalluria ranged from 1.5% to 72.2% in control subjects. An increase of urinary citrate excretion from 0.5 to 5 mmol/l significantly lowered the frequency of crystalluria from 32.4% to 10.1% for a pCaOx between 1 and 2 (mmol/l)2 (p < 0.0001) and from 63% to 27.9% for a pCaOx between 2 and 3 (mmol/l)2 (p < 0.001). For pCaOx values > or = 3 (mmol/l)2, urinary citrate excretion no longer significantly influenced the frequency of crystalluria. The number of crystals and aggregates and the maximum dimensions of aggregates were only influenced by the urinary citrate concentration when the pCaOx product was < 2 (mmol/l)2. CONCLUSION: The main determinant of the frequency and characteristics of weddellite crystalluria is the pCaOx molar product. The beneficial effect of the urinary citrate concentration on the frequency of crystalluria is observed for pCaOx values < 3 (mmol/l)2, but only for pCaOx values < 2 (mmol/l)2 for the characteristics of crystalluria such as the number and dimensions of crystals and aggregates. This means that therapeutic measures designed to increase urinary citrate concentrations can only be effective when pCaOx has been previously lowered by increased diuresis or specific reduction of urinary calcium and/or urinary oxalate levels.

Calcium↗
PubMed1991

[Comparative study between the anti-lithogenic action of zinc and copper against oxalic lithiasis in the rat].

Intraperitoneal injection of sodium oxalate, at the dose of 8 mg/100 g of body weight, induced into rats oxalate and calcium deposits in renal tissue, compared to animals which received distilled water (respectively P less than 0.05; P less than 0.05). However, when a zinc solution was administered previously, at the dose of 24 micrograms/100 g of body weight, oxalate and calcium accumulation was found to be significantly lower than in the group treated exclusively with sodium oxalate. Similar results were found when the metal used was copper, but oxalate accumulation was found to be significantly higher in this group than in the group treated with zinc (P less than 0.01). Compared to reference animals, which received distilled water, oxalate accumulation was found to be significantly decreased in the groups treated with both zinc (P less than 0.001) and copper (P less than 0.01), whereas calcium accumulation was found to be similar. Microscopic examination showed calcium crystals only in the group treated with sodium oxalate, preferentially localized in the renal papilla. These results suggest that zinc and copper, when administered at the dose of 24 mu/100 g of body weight, completely protect against experimental lithiasis induced by oxalic acid. However, the inhibitory effect of zinc was more pronounced than that of copper, especially against oxalate accumulation.

Animals↗