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PubMed1994

[Estimation of 24-h excretion of some promotors and inhibitors of crystallization and degree of urine saturation with calcium oxalate in calcium urinary calculi].

UNLABELLED: The aim of the study was to estimate the renal citrate excretion in basal condition and to find out the relationship between their excretion and excretion of calcium, oxalate, magnesium and phosphate in patients with calcium stone disease and in control group. In 93 patients with urolithiasis and 46 healthy subjects 24-h excretion of calcium, magnesium, oxalate, phosphate and citrate as well as the degree of urine saturation with calcium oxalate was evaluated. 24-h renal excretion of calcium was significantly higher in patients with urolithiasis than in control group (p < 0001). Excretion of magnesium, phosphate and oxalate were'nt significantly different between patients with urolithiasis and healthy subjects. Daily excretion of citrate was significantly lower in patients with calcium stone disease (p < 0.01) and the degree of urine saturation with calcium oxalate was significantly higher in this group (p < 0.001). Hypocitraturia was observed in 61.3% stone-formers. A significant positive correlation was observed between excretion of citrate and calcium (r = 0.2760 p < 0.01) as well as citrate and oxalate (r = 0.5310 p < 0.001) in patients with urolithiasis. CONCLUSIONS: 1. In 61.3% of patients with urolithiasis the daily citrate excretion was reduced. In 50% of patients with urolithiasis and reduced citrate excretion "idiopathic" hypocitraturia was recognized. The daily citrate excretion was reduced in 70.2% of stone-formers with infected urine. 2. The positive correlation between 24-h excretion of calcium and citrate suggests that high excretion of lithogenic factor is accompanied by high excretion of this inhibitor of crystallization.

Adult↗
PubMed1993

Thresholds of serum calcium oxalate supersaturation in relation to renal function in patients with or without primary hyperoxaluria.

Systemic oxalosis is a constant feature in patients with primary hyperoxaluria type 1 (PH1) and chronic renal failure (CRF) and is not prevented by regular dialysis (RDT), because removal cannot keep up with retention and overproduction of oxalate. These patients are candidates to kidney and/or liver transplantation, which should be ideally planned prior to the development of oxalosis. However, methods to detect the presence and extent of oxalosis are invasive and poorly reproducible, and only indirect approaches are feasible. Because supersaturation of body fluids is an essential condition for oxalotic deposits to form, we have assessed serum calcium oxalate saturation (beta CaOx) in 12 patients with PH1 and 26 with PH1-unrelated renal diseases and varying degrees of CRF. Nineteen healthy individuals were taken as controls. beta CaOx was closely dependent on oxalate serum levels. Serum oxalate and beta CaOx were increased in patients with CRF as compared to controls, and were inversely related to GFR, assessed as creatinine clearance. However, at any level of GFR, both were always greater in PH1 patients. From the slopes of the regression of beta CaOx over ClCr, saturation was predicted to be obtained at ClCr ranging 24-34 and 8-11 ml/min/1.73 m2 in PH1 and non-PH1 patients respectively. Based on the dependence of beta CaOx on oxalate, saturation was associated with serum oxalate between 44 and 46 mumol/l, irrespective of either the prevailing GFR or the underlying disease. These simple procedures represent a valuable non-invasive tool to define the risk of systemic oxalosis and may assist in timing of transplantation.

Adolescent↗
PubMed1993

Effects of citrate on the different phases of calcium oxalate crystallization.

Urinary citrate appears to be an important factor in the crystallization process of calcium oxalate and calcium phosphate. The urinary excretion of citrate was found to be significantly lower in patients with calcium oxalate stone disease as compared with normal subjects, and about 30 per cent of the calcium stone formers can be considered as hypocitraturic. The lowest excretion of citrate was recorded in urine collected during the night. Citrate has significant effects on supersaturation with respect to both calcium oxalate and calcium phosphate, it also inhibits the growth of these crystals. In addition, citrate appears to be capable of inhibiting the aggregation of crystals composed of calcium oxalate, brushite, and hydroxyapatite. The heterogenous growth of calcium oxalate on calcium phosphate is also counteracted by citrate. As a consequence of the crucial role of citrate in these processes, stone prevention with alkaline citrate has become an attractive form of treatment in patients with recurrent stone formation. Single evening dose administration of sodium potassium citrate resulted in an of sodium potassium citrate resulted in an increased excretion of citrate, reduced levels of the calcium/citrate ratio as well as supersaturation with respect to calcium oxalate and a decreased rate of stone formation. However, conflicting results of stone preventive treatment with alkaline citrate have been reported by different groups, and long-term follow-up of patients treated in a randomized way is necessary to definitely assess the efficacy of alkaline citrate.

Calcium Oxalate↗
PubMed1993

[Effect of verapamil on urinary calcium and oxalate excretion in renal stone formers].

The effect of the calcium antagonist verapamil on urinary calcium and oxalate excretion was examined and compared with that of trichlormethiazide to evaluate whether verapamil is useful in the prevention of calcium oxalate renal stones. Twenty-four-hour urine of 16 renal stone formers was measured at the outpatient clinic before and after administration of 120 mg/day verapamil for a mean duration of 2.7 months (range, 2 weeks to 6 months). The 24-hour urine was analyzed for creatinine, calcium, oxalic acid, magnesium and citric acid and the results compared with those in 20 renal stone formers who were administered trichlormethiazide. Verapamil was found to significantly reduce the urinary oxalate excretion of the 5 hyperoxaluric (> or = 50 mg/day) patients but no significant effect on urinary calcium, magnesium or citric acid was observed. Conversely, trichlormethiazide significantly decreased urinary calcium excretion in the hypercalciuric (> or = 250 mg/day) patients. Calcium oxalate risk index of hypercalciuric and hyperoxaluric patients was significantly reduced after the administration of verapamil. These findings suggest that verapamil is effective in reducing urinary oxalate excretion in the hyperoxaluric patients.

Calcium↗
PubMed1977

Estimation of the state of saturation of brushite and calcium oxalate in urine: a comparison of three methods.

The estimation of the degree of saturation of brushite and of calcium oxalate in urine of patients with disorders of calcium metabolism has been proved to be an effective tool in evaluating the patient's propensity to form renal stones. The methods used in three different laboratories have been compared and evaluated in 27 urine samples. Relative saturation ratio (ratio of activity product and thermodynamic solubility product of brushite) and activity product ratio (ratio of activity product of original sample and that obtained after incubation of sample with synthetic brushite) were determined. Similar studies were performed for calcium oxalate. The values for relative saturation ratio of brushite or calcium oxalate differed widely among the three techniques. However, nearly identical values for activity product ratio of brushite were obtained. The activity product ratios of calcium oxalate, obtained by different techniques, closely approximated each other except in sampels containing excessive amounts of calcium (greater than 5 mM) or oxalate (greater than 5 mM). The values for the relative saturation ratios for both brushite and calcium oxalate were usually higher than the corresponding values for activity product ratio. The results indicate that the use of activity product ratio provides a more simple and reliable estimate of the urinary state of saturation than does the relative saturation ratio.

Ammonia↗
PubMed1996

[Uronic-acid-rich protein: a new glycoprotein inhibiting the crystallization of calcium oxalate in vitro].

During about ten years, nephrocalcin was considered the main calcium oxalate crystal growth inhibitor. Today, it appears only a urinary protein inhibitor among other ones such as non polymerized Tamm-Horsfall protein, uropontin or crystal matrix protein (CMP), a protein derived from prothrombin. All these molecules are able to inhibit either crystal growth or aggregation of calcium oxalate in urine. Another protein, named renal lithostathine, was also reported to be a potent inhibitor of secondary nucleation and growth of calcium carbonate crystals. A new urinary inhibitor of calcium oxalate formation was isolated from the urine of healthy subjects using chromatographic procedures. It is a macromolecule with a molecular weight (MW) of approximately 35 kDa as estimated by polyacrylamide gel electrophoresis. Its carbohydrate content represents an average of 8.5% of its MW. Glutamic and aspartic acids represent 24% of total amino acids. This protein is called Uronic-Acid-rich Protein (UAP) because of its uronic acid content. The same protein isolated from the urine of stone formers showed less inhibitory activity than that purified from the urine of healthy subjects. Structural modifications may explain this diminution of its inhibitory activity. This protein was also purified from rat urine using same procedures. Human and rat UAP exhibit similar biochemical characteristics and strongly inhibit calcium oxalate crystallization in vitro. Partial amino acid sequence analysis showed a homology with inter-alpha-trypsin inhibitor (ITI), confirmed by the immunological results on Western blot. Nevertheless, various chemical and enzymic treatments revealed that UAP and ITI are not identical molecules. Consequently, urine contains several macromolecular substances belonging to ITI superfamily which are involved in the inhibition of calcium oxalate crystallization. UAP takes place among the most efficient macromolecular substances known as inhibitors in calcium oxalate nephrolithiasis.

Animals↗
PubMed1997

Urinary calcium oxalate saturation in healthy infants and children.

PURPOSE: A number of factors influence the development of renal calculi, the most essential of which is the supersaturation of urine with lithogenic substances. Calcium oxalate stones occur most frequently in adult and pediatric patients with urolithiasis. Therefore, we established normal age and sex related data for urinary calcium oxalate saturation in infancy and childhood to allow a more specific prediction of the risk of (recurrent) stone disease. MATERIALS AND METHODS: We collected 24-hour urine samples from 473 healthy infants and children without a history of renal stones. Urinary lithogenic and stone inhibitory substances were measured, and the urinary calcium oxalate saturation was calculated using a computer program. RESULTS: Mean urinary calcium oxalate saturation was always higher in boys than in girls, which was significant in infancy (5.22 versus 2.03, p < 0.05) and at ages 7 to 9 years (8.84 versus 5.47, p < 0.05). The saturation first increased (p < 0.05) until age 7 to 9 years in boys and girls, and remained at high levels at ages 10 to 12 years (7.03 versus 5.49, p < 0.05 compared to infancy). Calcium oxalate saturation then decreased until adolescence when values were comparable to those of infancy (5.29 versus 3.35). CONCLUSIONS: We recommend calculating urinary calcium oxalate saturation for diagnostic purposes as well as for therapy control. Normal age and sex related values must be considered.

Adolescent↗
PubMed1982

Oxalate metabolism and renal calculi.

Changes in oxalate excretion (together with changes in urinary volume) constitute the most important factors in altering the probability of renal stone formation. However, investigations on oxalate metabolism have been sparse, perhaps because of the lack of an accurate method for measuring oxalate in biologic fluids. Available data clearly implicate increased urinary oxalate excretion as the etiological factor in stone formation in two groups of patients--those with primary hyperoxaluria and those with gastrointestinal malabsorption. Evidence for the existence of hyperoxaluria in the patient with the "garden" variety of calcium oxalate stones is less persuasive.

Animals↗
PubMed1989

Transient hyperoxaluria after ingestion of chocolate as a high risk factor for calcium oxalate calculi.

In 6 male subjects the diurnal variation of urinary oxalic acid excretion was studied after ingestion of chocolate, a food stuff rich in oxalic acid. The ingestion of chocolate caused a striking but transient increase in urinary oxalic acid excretion due to its absorption in the upper gastrointestinal tract. The peak excretion rates occurred 2-4 h after the intake of the chocolate. The peak values were 235% of the fasting excretion rate in the trial with 50 g chocolate and 289% in the trial with 100 g chocolate and reached the amounts found in cases with primary hyperoxaluria. The administration of ranitidine had no influence on oxalic acid absorption. The transient hyperoxaluria observed seems to be an important factor for the formation of calcium oxalate calculi in patients on risk for stone disorders.

Adult↗
PubMed1988

The bioavailability of calcium in spinach and calcium-oxalate to calcium-deficient rats.

We estimated the utilization of calcium in spinach and calcium-oxalate to calcium-deficient rats, and the effect of oxalic acid on absorption of dietary calcium by using calcium-deficient rats. The body weight gain of the calcium-deficient rats for 8 days receiving a calcium-deficient diet supplemented with raw-powdered spinach (R-sp), boiled-powdered spinach (B-sp), or calcium-oxalate (Ca-ox), and a control diet supplemented with oxalic acid (OX-C) were 4.8, 2.8, 4.9, and 5.1 g, respectively. The calcium content in the liver and kidney of the rats receiving R-sp, B-sp, Ca-ox, and OX-C diets significantly increased as compared with the calcium-deficient rats. Significant differences in the liver calcium levels were not observed among the rats receiving various additional diets, though the content in the kidneys of the rats receiving R-sp, B-sp, Ca-ox, and OX-C diets were 28.0, 21.5, 0.11, and 0.59 mg, respectively. An especially large amount of calcium was accumulated in the kidneys of the rats receiving R-sp and B-sp diets. The calcium concentration in the serum of the rats receiving Ca-ox and OX-C diets was higher than the calcium concentration in the serum of the R-sp, B-sp, and calcium-deficient rats. The calcium content in the left tibiae of the rats receiving Ca-ox and OX-C diets was higher than that of the rats receiving R-sp and B-sp diets. The breaking force of the right tibiae of the rats was highest in the OX-C group, and higher in the R-sp and Ca-ox groups than the breaking force of the right tibiae of the rats fed on B-sp diet. The alkaline phosphatase activity in the small intestines of the rats rose in the order of the R-sp, B-sp, and Ca-ox groups, although significant differences of the activity were not observed between the Ca-ox and the OX-C groups. The calcium retention of the rats receiving the calcium-deficient, R-sp, B-sp, Ca-ox, and OX-C diets was -18.5, 35.2, 25.6, 41.6, and 45.8%, respectively. About 35% of the calcium in the spinach was absorbed by the calcium-deficient rats, and oxalic acid depressed the calcium absorption in the rats.

Absorption↗
PubMed1987

Two-carbon oxalogenesis compared in recurrent calcium oxalate stone formers and normal subjects.

We used a xylitol load to test the two-carbon pathway to oxalate production in humans. Use of this pentose sugar caused a fourfold increase in glycolate excretion, indicating its suitability as a dynamic function test of two-carbon metabolism. However, despite this increase in glycolate excretion in 10 recurrent stone formers and six normal subjects, there was no concomitant increase in oxalate excretion in either group. By comparison, a sucrose load produced no increase in excretion of either glycolate or oxalate. In addition, when we studied four recurrent calcium stone formers on successive diets with various fat content, we found no correlation between high fat intake and increased glycolate or oxalate excretion. In summary, there was no evidence of abnormal fluxes through the two-carbon pathway to oxalate in recurrent stone formers, nor of hyperoxaluria as related to increased intake of sucrose or fat.

Adult↗
PubMed1983

Pyridoxine therapy in patients with renal calcium oxalate calculi.

In 12 patients with idiopathic calcium oxalate calculi pyridoxine was administered. Within six weeks mean daily oxalic acid excretion decreased from 480 +/- 122 mumol to 336 +/- 83 mumol. Glycolic acid excretion fell from 208 +/- 51 mumol to 153 +/- 26 mumol (normal range: oxalic acid 228-412 mumol/day, glycolic acid 130-290 mumol/day). The reduction of oxalic acid excretion seems to be beneficial in prevention of idiopathic calcium oxalate calculi.

Calcium Oxalate↗
PubMed1991

Involvement of serotonergic neuronal systems in the anti-amnesic action of naftidrofuryl oxalate.

The effects of naftidrofuryl oxalate on cycloheximide- and 5-hydroxytryptophan (5-HTP)-induced amnesia were investigated using a passive avoidance task in mice. Naftidrofuryl oxalate significantly improved the cycloheximide-induced amnesia. This effect of naftidrofuryl oxalate was antagonized by 5-HTP, a serotonin (5-HT) precursor, and by p-chloroamphetamine (PCA), a 5-HT releaser. Single administration of 5-HTP in combination with pargyline, a monoamine oxidase inhibitor, induced amnesia (5-HTP-induced amnesia). This amnesia was attenuated by ritanserin, a 5-HT2-selective antagonist, but not by pindolol, a 5-HT1-selective antagonist. Naftidrofuryl oxalate also attenuated the 5-HTP-induced amnesia. A binding study revealed that naftidrofuryl oxalate inhibited the binding of [3H]ketanserin to 5-HT2 receptors in mouse brain synaptic membrane in a dose-dependent fashion (IC50 = 1.42 x 10(-7) M), but did not inhibit that of [3H]serotonin to 5-HT1 receptors. These results suggest that naftidrofuryl oxalate may attenuate cycloheximide- and 5-HTP-induced amnesia by blocking 5-HT2 receptor subtypes.

Amnesia↗
PubMed1991

Naftidrofuryl oxalate, nootropic effects on the scopolamine- and the basal forebrain lesion-induced amnesia in rats.

We studied the effects of naftidrofuryl oxalate on scopolamine- and basal forebrain (BF) lesion-induced amnesia using passive avoidance and multiple T-maze tasks, in comparison with Ca-hopantenate and physostigmine in rats. In the passive avoidance task, one-week treatment with naftidrofuryl oxalate (12.5 and 25 mg/kg, IP) ameliorated BF lesion-induced amnesia. The multiple T-maze task was done with two training sessions per day for five continuous days. We measured the number of errors made from start box to goal box. Naftidrofuryl oxalate (12.5 mg/kg, IP, b.i.d.) and physostigmine (0.1 mg/kg, IP, b.i.d.) attenuated scopolamine- and BF lesion-induced amnesia. However, treatment with naftidrofuryl oxalate for one week failed to inhibit the decrease of the choline acetyltransferase induced by the BF lesion. Ca-hopantenate did not show attenuation of amnesia induced by the scopolamine or BF lesion. These results suggest that naftidrofuryl oxalate enhances the storage of spatial information, and that the nootropic effects of naftidrofuryl oxalate may be produced by an indirect activation of the cholinergic system through serotonergic neuronal systems.

Amnesia↗
PubMed2005

An ATR-FTIR spectroscopic study of the competitive adsorption between oxalate and malonate at the water-goethite interface.

The competitive adsorption between oxalate and malonate at the water-goethite interface was studied as a function of pH and total ligand concentrations by means of quantitative adsorption measurements and attenuated total reflectance Fourier transform infrared (ATR-FTIR) spectroscopy. The results obtained show that ATR-FTIR spectroscopy resolves the individual spectroscopic features of oxalate and malonate when adsorbed simultaneously at the water-goethite interface. The characteristic peaks of all four types of predominating surface complexes existing in the single ligand systems were identified, namely one inner sphere and one outer sphere surface complex for each ligand. The quantitative adsorption data showed that oxalate partially out-competes malonate at the water-goethite interface. Evaluation of the peak area variations as a function of pH indicated that the stronger oxalate adsorption can be ascribed to the more stable inner sphere surface complex of oxalate, which in turn is related to the oxalate five-member chelate ring structure yielding a more stable complex compared to the six-member ring of malonate.

Journal Article↗
PubMed2004

Heterogeneous photocatalytic reduction of chromium(VI) over TiO2 particles in the presence of oxalate: involvement of Cr(V) species.

Cr(VI) photocatalytic reduction experiments over TiO2 particles under near UV irradiation in the presence of excess oxalate were performed at acid pH (2 and 3) and under air and N2 bubbling. Initial photonic efficiencies for Cr(VI) reduction are nearly the same under aerobic and anaerobic conditions, but show a significant increase at the lowest pH. At pH 2, the addition of oxalate facilitates Cr(VI) reduction, hindering the electron-shuttle mechanism taking place in pure water. The oxalate synergistic effect at pH 2 is lower than that previously found for EDTA and negligible at pH 3. Chromium(V) oxalate concentration profiles were obtained by EPR spectroscopy in the presence of excess oxalate at pH 1.5. Coordinated Cr(V) complexes [Cr(V)(O)(Ox)2]-, [Cr(V)(OH2)(Ox)2]-, and [Cr(V)(O)(OH)2(Ox)]- were identified, on the basis of the comparison of their corresponding g values with recent literature data. The kinetic analysis of the temporal evolution of the paramagnetic Cr(V) species indicates also an effective photocatalytic degradation of chromium(V) oxalate complexes. This new evidence reinforces previous findings regarding sequential one-electron-transfer processes in Cr(VI) photocatalytic reduction, suggesting that this route may represent a general behavior for the Cr(VI) reduction over UV-irradiated TiO2 particles.

Carcinogens, Environmental↗
PubMed1998

Molecular characterization of the oxalate oxidase involved in the response of barley to the powdery mildew fungus.

Previously we reported that oxalate oxidase activity increases in extracts of barley (Hordeum vulgare) leaves in response to the powdery mildew fungus (Blumeria [syn. Erysiphe] graminis f.sp. hordei) and proposed this as a source of H2O2 during plant-pathogen interactions. In this paper we show that the N terminus of the major pathogen-response oxalate oxidase has a high degree of sequence identity to previously characterized germin-like oxalate oxidases. Two cDNAs were isolated, pHvOxOa, which represents this major enzyme, and pHvOxOb', representing a closely related enzyme. Our data suggest the presence of only two oxalate oxidase genes in the barley genome, i.e. a gene encoding HvOxOa, which possibly exists in several copies, and a single-copy gene encoding HvOxOb. The use of 3' end gene-specific probes has allowed us to demonstrate that the HvOxOa transcript accumulates to 6 times the level of the HvOxOb transcript in response to the powdery mildew fungus. The transcripts were detected in both compatible and incompatible interactions with a similar accumulation pattern. The oxalate oxidase is found exclusively in the leaf mesophyll, where it is cell wall located. A model for a signal transduction pathway in which oxalate oxidase plays a central role is proposed for the regulation of the hypersensitive response.

Amino Acid Sequence↗
PubMed1991

Production and degradation of oxalic Acid by brown rot fungi.

Our results show that all of the brown rot fungi tested produce oxalic acid in liquid as well as in semisolid cultures. Gloeophyllum trabeum, which accumulates the lowest amount of oxalic acid during decay of pine holocellulose, showed the highest polysaccharide-depolymerizing activity. Semisolid cultures inoculated with this fungus rapidly converted C-labeled oxalic acid to CO(2) during cellulose depolymerization. The other brown rot fungi also oxidized C-labeled oxalic acid, although less rapidly. In contrast, semisolid cultures inoculated with the white rot fungus Coriolus versicolor did not significantly catabolize the acid and did not depolymerize the holocellulose during decay. Semisolid cultures of G. trabeum amended with desferrioxamine, a specific iron-chelating agent, were unable to lower the degree of polymerization of cellulose or to oxidize C-labeled oxalic acid to the extent or at the rate that control cultures did. These results suggest that both iron and oxalic acid are involved in cellulose depolymerization by brown rot fungi.

Journal Article↗