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PubMed1988

Evidence for a cytoplasmic pathway of oxalate biosynthesis in Aspergillus niger.

Oxalate accumulation of up to 8 g/liter was induced in Aspergillus niger by shifting the pH from 6 to 8. This required the presence of Pi and a nitrogen source and was inhibited by the protein synthesis inhibitor cycloheximide. Exogenously added 14CO2 was not incorporated into oxalate, but was incorporated into acetate and malate, thus indicating the biosynthesis of oxalate by hydrolytic cleavage of oxaloacetate. Inhibition of mitochondrial citrate metabolism by fluorocitrate did not significantly decrease the oxalate yield. The putative enzyme that was responsible for this was oxaloacetate hydrolase (EC 3.7.1.1), which was induced de novo during the pH shift. Subcellular fractionation of oxalic acid-forming mycelia of A. niger showed that this enzyme is located in the cytoplasm of A. niger. The results are consistent with a cytoplasmic pathway of oxalate formation which does not involve the tricarboxylic acid cycle.

Aspergillus niger↗
PubMed1975

Regional differences in oxalate absorption by rat intestine: evidence for excessive absorption by the colon in steatorrhoea.

Clinical studies suggest that steatorrhoea can be associated with excessive absorption of dietary oxalate. We examined the influence of bile salts, Ca++, and long-chain fatty acid on the absorption of oxalate and water by rat intestine in vivo. Absorption was measured under steady-state conditions during single-pass infusions. Each intestinal segment served as its own control. In jejunum, 10 mM taurocholate, the principal salt in rat bile, depressed absorption of oxalate and water. Absorption was not depressed further by Ca++ or linoleic acid. In ileum, 10 mM taurocholate did not inhibit absorption. Linoleic acid, 2 mM, depressed absorption of both oxalate and water. In colon 10 mM taurocholate decreased absorption. Net water transport was depressed further when linoleic acid was added to the infusion, but oxalate absorption was enhanced. Ca++ negated these effects of linoleic acid. It is concluded that long-chain fatty acids may enhance the absorption of oxalate from the rat colon. This observation may be relevant to understanding hyperoxaluria in patients with steatorrhoea.

Animals↗
PubMed1998

Effects of sulfate and chloride on three separate oxalate transporters reconstituted from rabbit renal cortex.

Understanding the mechanism of sulfate-dependent, oxalate-stimulated chloride reabsorption in the mammalian proximal tubule is complicated by the presence of multiple oxalate and sulfate transport pathways. Accordingly, we developed a method of reconstituting functional oxalate transport from the rabbit renal cortex so that the individual transporters might be examined. Solubilized microvillus membrane proteins were separated by hydroxyapatite chromatography and then reconstituted into proteoliposomes. Two peaks of oxalate/oxalate exchange activity were observed. Sulfate (10 mM) cis-inhibits oxalate transport in the early peak by 93% and in the later peak by 41%. In contrast, 20 mM chloride inhibits oxalate/oxalate exchange by only 32% in the early peak but inhibits oxalate exchange by 70% in the later peak. Oxalate-stimulated sulfate uptake was observed in the early fractions but not in the later fractions. These data are consistent with the recovery of the sulfate/oxalate exchanger in the early hydroxyapatite fractions and the chloride/oxalate exchanger in the later fractions. The basolateral membrane sulfate/oxalate exchanger was also reconstituted. The reconstituted basolateral and apical membrane sulfate/oxalate exchangers demonstrate nearly identical patterns of substrate specificities. However, 98% of apical sulfate/oxalate exchange activity is lost following exposure to octylglucoside at room temperature, whereas the basolateral sulfate/oxalate exchange activity was reduced 67% (P < 0.05). In conclusion, functional reconstitution of solubilized membrane proteins demonstrates that apical membrane chloride/oxalate exchange and sulfate/oxalate exchange are mediated by different transport proteins. Apical and basolateral sulfate/oxalate exchange may also represent transport on two separate exchangers.

Animals↗
PubMed1987

Oxalate dynamics in chronic renal failure. Comparison with normal subjects and patients with primary hyperoxaluria.

In order to separate the effect of oxalate retention in primary hyperoxaluria with renal failure from that of excessive oxalate synthesis and to determine the optimum time for renal transplantation in primary hyperoxaluria, we have studied a series of patients with different degrees of renal failure due to other causes. The results were compared with those obtained in studies on 8 patients with primary hyperoxaluria at different levels of residual overall renal function. In the patients with renal failure unrelated to primary hyperoxaluria, oxalate retention increases rapidly when the glomerular filtration rate (GFR) decreases below about 20 ml X min-1. These results suggest that the reduced renal excretory contribution to oxalate accumulation in primary hyperoxaluria would be expected to be particularly important in this range of GFR. In primary hyperoxaluria, oxalate retention occurs when GFR is only a little below the reference range and measures to remove oxalate from the body should be considered when the GFR falls below 40 ml X min-1 X 1.73 m-2, with a view to their introduction when the GFR is in the range 20-25 ml X min-1 X 1.73 m-2.

Carbon Radioisotopes↗
PubMed1997

Induction of renal nuclear oxalate binding activity in experimental hyperoxaluric rats.

The hyperoxaluric rat kidney nucleus exhibited a 50% increase in oxalate binding activity of control in both the residual fraction containing nuclear envelopes and the histone fraction with a concomitant increase in basal lipid peroxidation and a decrease in thiol content. However, in vitro lipid peroxidation induced by the ascorbate-ADP-Fe3+ system increased the oxalate binding activity of the residual fraction with a positive correlation but inhibited the histone oxalate binding activity with a negative correlation with depletion of thiols during peroxidation in both control and hyperoxaluric rats. A twofold increase in oxalate concentration was observed in the nucleus as well as the nuclear subfractions in hyperoxaluria. Hyperoxaluric rat kidneys showed increased H1 and oxalate binding activity, and the distribution of H1B was higher than that in the control. The present study suggests that the increased nuclear oxalate binding activity in hyperoxaluric rats was not due to lipid peroxidation but due to increased formation of histone H1.

Animals↗
PubMed1990

Relation between calcium oxalate hydrate form found in renal calculi and some urinary parameters.

In calcium oxalate urolithiasis, the monohydrate and dihydrate forms can be found. The aim of this paper is to examine a group of patients with calcium oxalate calculi to determine the calcium oxalate form and the possible relationship with calcium and other urinary biochemical parameters. It was found that calcium oxalate monohydrate is more frequent in the normocalciuric group and also is associated with a lack of inhibitory capacity, while a mixed calculus of calcium oxalate and phosphate or calcium oxalate dihydrate can be related with hypercalciuria.

Calcium↗
PubMed1997

Measurement of metastability, growth and aggregation of calcium oxalate in native urine. A new approach for clinical and experimental stone research.

Nucleation, growth and aggregation are thought to be the most important crystallization processes in stone formation. Since crystallization properties change with urinary dilution, centrifugation and filtration, crystallization should always be studied in freshly voided and not pretreated urine. Recently we developed an automated method where calcium oxalate crystallization is induced in native urine by an exogenous oxalate load and nucleation and growth are monitored by an ion-selective calcium electrode. The method has now been supplemented with the spectrophotometric measurement of crystal aggregation. Repeated experiments in the same urine with different oxalate loads enable the determination of the critical oxalate additionable to induce crystallization (metastable limit) and the calculation of an oxalate load-independent growth rate constant. Preliminary results obtained in the native urine of healthy controls showed an extremely high limit of metastability and a complete absence of crystal aggregation. These findings may explain why, despite frequent urinary calcium oxalate supersaturation, healthy people do not form stones.

Calcium Oxalate↗
PubMed1992

Pulmonary oxalate deposition associated with Aspergillus niger infection. An oxidant hypothesis of toxicity.

Tissue injury by Aspergillus niger infection is associated with the deposition of calcium oxalate crystals. Oxalate is recognized to function as a ligand for numerous metal cations and will react with ferric ion to form a coordination complex. We describe oxalate deposition in the lung of a patient with A. niger infection and quantify surface-complexed Fe3+. Crystals collected from lung tissue demonstrated considerable concentrations of surface iron. In addition, we tested the hypothesis that this surface coordination of Fe3+ by oxalate is associated with increased in vitro oxidant generation. Calcium oxalate crystals (1.0 mg/ml) complexed all available Fe3+ from solutions of ferric chloride to concentrations of as much as 1.0 mM. Oxidant generation in both a chemical and a cellular system, measured as thiobarbituric-acid-reactive products of deoxyribose and chemiluminescence, respectively, increased with coordination of higher concentrations of inorganic iron. We conclude that calcium oxalate associated with A. niger infection complexes iron cations onto the crystalline surfaces and may generate oxidants at the solid-solution interface, which could result in tissue injury.

Aspergillosis↗
PubMed1993

Comparison of a commercial enzymic kit for urinary oxalate analysis with a high performance liquid chromatographic method.

A new commercial enzymic kit for urinary oxalate determination has been adapted for use on a centrifugal analyser. It has been evaluated and compared with an established high performance liquid chromatographic (HPLC) procedure developed in our laboratory. Mean recovery of oxalate from urine samples augmented with oxalic acid exceeded 97% by both methods. The precision of the HPLC method was superior to that of the enzymic kit but both methods gave between batch precision values better than CV 12% at low (less than 100 mumol/L) oxalate concentrations and better than CV 7% at higher concentrations (greater than 270 mumol/L). Urinary oxalate values obtained with the new enzymic procedure correlated more closely with HPLC values (r = 0.84) than did values previously obtained using the forerunner of the kit (r = 0.62) which was known to be susceptible to ascorbate interference. No significant interference from ascorbic acid or from high urinary calcium concentrations could be demonstrated using either the improved kit or the HPLC procedure. Its easy adaptation to automated analysers available in most laboratories, coupled to its acceptable analytical performance render the enzymic kit a reasonable alternative to HPLC or other more complex procedures for urinary oxalate analysis.

Chromatography, High Pressure Liquid↗
PubMed2002

Efficient synthesis and hydrolysis of cyclic oxalate esters of glycols.

Based on the mechanism postulated for the formation of the cyclic carbonates 3 in the reactions of glycols 1 with oxalyl chloride in the presence of triethylamine, we present here three efficient syntheses of the cyclic oxalates 2 of various glycols 1 by controlling the formation of 3: replacement of the base by pyridine markedly diminishes yields of 3 in all reactions, realizing dramatic reversals of the product ratios in the reactions with the (R*,R*)-compounds 1g-i,q,r and pinacol (1k); although considerable amounts of the oxalate polymers are formed in the reactions with some (R*,S*)-glycols, this drawback can be removed by the use of 2,4,6-collidine instead of pyridine; 1,1'-oxalyldiimidazole is useful for the synthesis of two selected cyclic oxalates 2e,f. The cyclic oxalates 2 other than trisubstituted and tetrasubstituted ones were found to be very reactive: kinetic studies on the hydrolysis of 1,4-dioxane-2,3-dione (2a) as well as its mono- and some selected 5,6-disubstituted derivatives 2 have revealed that they undergo hydrolysis 260-1500 times more rapidly than diethyl oxalate (12) in acetate buffer-acetonitrile (pH 5.69) at 25 degrees C. Although the cyclic oxalate 21 from cis-1,2-cyclopentanediol (11) was 1.5 times more reactive than 2a, it has been shown with other substrates that increasing number of the alkyl substituents decreases the rate of hydrolysis. On the contrary, the phenyl group was found to have somewhat accelerative effect.

Esters↗
PubMedDate not supplied

Changes in calcium oxalate crystal morphology as a function of supersaturation.

PURPOSE: To study the changes in calcium oxalate crystal morphology induced by different levels of supersaturation (SS) in human urine. MATERIALS AND METHODS: Twenty-four hours urine samples from 5 normal men were collected. Each specimen was centrifuged and filtered. About 200 mL of each sample was dialyzed overnight. Aliquots of 2 mL of urine was then added to a 24-wells tissue culture plate and checked for crystal absence. Calcium oxalate crystals were precipitated from each sample by adding sodium oxalate and calcium chloride in sufficient quantities to induce spontaneous crystallization. Finally, each plate hole was examined with an inverted polarized microscope (X500 magnification). Initial SS of each sample relative to calcium oxalate was calculated using an iterative computer program. RESULTS: Crystal formation was connected to relative calcium oxalate (CaOx) SS. At SS of 10, small crystals of similar shape were formed, mainly CaOx dihydrate morphology. At SS of 30, there was an enormous increase in the number of crystals, that kept the same size. SS greater than 50 produced larger crystals with different shapes and multiple crystalline aggregates. Urine was able to tolerate, i.e., to avoid crystal formation, until SS ratios of approximately 10. CONCLUSIONS: Relative CaOx SS and the concentration ratio of calcium to oxalate are important determinanting factors of crystal morphology. Non-dialyzable urinary proteins can act as inhibitors and influence the structure of formed crystals. Additional studies from patients with kidney stones are needed in order to establish whether crystal size and habit distribution are different from crystals in normal urine.

Calcium Oxalate↗
PubMed2005

In vitro evaluation of canine and feline calcium oxalate urolith fragility via shock wave lithotripsy.

OBJECTIVE: To test the hypothesis that feline calcium oxalate uroliths are intrinsically more resistant to comminution via shock wave lithotripsy (SWL) than canine calcium oxalate uroliths through comparison of the fragility of canine and feline uroliths in a quantitative in vitro test system. SAMPLE POPULATION: Calcium oxalate uroliths (previously obtained from dogs and cats) were matched by size and mineral composition to create 7 pairs of uroliths (1 canine and 1 feline urolith/pair). PROCEDURE: Uroliths were treated in vitro with 100 shock waves (20 kV; 1 Hz) by use of an electrohydraulic lithotripter. Urolith fragmentation was quantitatively assessed via determination of the percentage increase in projected area (calculated from the digital image area of each urolith before and after SWL). RESULTS: After SWL, canine uroliths (n = 7) fragmented to produce a mean +/- SD increase in image area of 238 +/- 104%, whereas feline uroliths (7) underwent significantly less fragmentation (mean image area increase of 78 +/- 97%). The post-SWL increase in fragment image area in 4 of 7 feline uroliths was < 50%, whereas it was > 150% in 6 of 7 canine uroliths. CONCLUSIONS AND CLINICAL RELEVANCE: Results indicate that feline calcium oxalate uroliths are less susceptible to fragmentation via SWL than canine calcium oxalate uroliths. In some cats, SWL may not be efficacious for fragmentation of calcium oxalate nephroliths or ureteroliths because the high numbers of shock waves required to adequately fragment the uroliths may cause renal injury.

Animals↗
PubMed1980

Oxalate content of some common foods: determination by an enzymatic method.

A specific enzymatic method was used to determine the oxalate content of some common foods. No preliminary isolation of oxalate was required and recoveries ranging from 95-110 per cent were obtained. Spinach, rhubarb, peanuts, chocolates, parsley and tea were found to contain high levels of oxalate as previously described by others. On the other hand the oxalate content of beetroot was found to be five times as high as previously reported, but coca-cola and beer were almost free from oxalate. Cereals and meat were either low or deficient in oxalate.

Beverages↗
PubMed1985

Urolithiasis in railroad shopmen in relation to oxalic acid exposure at work.

It is well known that the urinary excretion of oxalic acid is one of the main determinants for urinary stone formation. From 1950 to 1978 a saturated oxalic acid solution was used in a repainting and cleaning process for railroad cars in Norwegian railroad workshops. With the use of a questionnaire, the cumulative prevalence of urolithiasis-induced colic episodes was registered in the Sundland railroad depot. Forty-two (11.9%) out of 353 male workers not exposed to oxalic acid reported having had one or more such stone colic episodes. The corresponding figure for 15 individuals who had a very high exposure to oxalic acid was 8 (53.3%). Also workers in other departments, occasionally exposed to oxalic acid, had an increased stone colic prevalence rate, a finding suggesting a positive dose-response relationship. There was an increased frequency of stone colic episodes in the age group 40-69 years. Seven heavily exposed workers in the paint shop reported initial pollakiuria and slight dysuria during the exposure. The study indicates a causal relation between urinary stone formation in the investigated railroad shopmen and their exposure to oxalic acid at work.

Adult↗
PubMed2005

Ethylene glycol intoxication and xylitol infusion--metabolic steps of oxalate-induced acute renal failure.

Acute renal failure is a major complication in patients with increased oxalate serum concentration. To describe the metabolic mechanisms of oxalate-induced glomerular and tubular damage, we report a case of ethylene glycol intoxication as well as a case of xylitol infusion in a patient with previously unknown primary hyperoxaluria type 1. Both patients presented with acute renal failure associated with histologically proven renal oxalate accumulation. This excessive oxalate overloading resulted from elimination and metabolization of ethylene glycol or xylitol. Thus, key enzymes in the elimination pathway of these substances represent targets for pharmacological treatment. Simultaneous hemodialysis is often necessary to reduce oxalate serum concentration. Whereas renal function of the ethylene glycol-poisoned patient recovered, the second patient who received xylitol infusion required chronic hemodialysis due to the unmasked hyperoxaluria type 1. Our cases demonstrate that patients with excessive endogenous oxalate generation are at high risk to develop acute renal failure. Therefore, to prevent end-stage renal failure in these patients, important clinical factors should be considered as indicators for the underlying cause: history of alcohol abuse and severe high anion gap acidosis for ethylene glycol intoxication or history of long-lasting parenteral nutrition for xylitol-associated acute renal failure.

Acute Kidney Injury↗
PubMed1989

[The quantitative study of inhibitory effect of pentosan polysulfate and chlorophyllin on the experimental calcium oxalate stone].

The purpose of this study is to evaluate the effect of sodium pentosan polysulfate (SPP) and sodium copper chlorophyllin (SCC) on the formation, growth and aggregation of calcium oxalate crystals in vivo, and to measure the number and the volume of crystals formed in the rat kidney, quantitatively, with a Coulter counter TA-II. The deposition of calcium oxalate crystals in the rat kidney was induced by intraperitoneal injection of 2.5 g per Kg of body weight of hydroxy-L-proline and administration of 0.4% ethylene glycol as the drinking fluid ad libitum for 7 days. Daily excretions of urinary oxalate, calcium (ratio to urinary creatinine) and urinary volume were measured. Both kidneys were removed after protocol. The kidneys were homogenized with 0.2 M Tris-buffer (pH 8.0) and subsequently digested in soluene-100. After calcium oxalate crystals were collected, they were suspended in saline saturated with calcium oxalate. The crystal size distribution was measured with a Coulter counter TA-II. In addition, the renal calcium content was measured by atomic absorption spectrometry, and the kidneys were examined by optical microscopy and scanning electron microscopy. The crystals formed in the rats' kidneys were analyzed by infrared spectroscopy. The results were as follows: 1. There was no deposition of crystals in the kidney of the rats which were not treated. There was intratubular deposition of crystals in the kidneys of the rats injected with hydroxy-L-proline and administered 0.4% ethylene glycol. They consisted of calcium oxalate monohydrate. 2. Renal calcium content was significantly higher in the groups with induced crystals than the control group.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

[Some effects of pH, diuretics and organic acids on the uptake of oxalate in a renal tubular cell line (LLC-PK1)].

The effects of changes in extracellular pH and treatments with diuretics or some organic acids on the uptake of oxalate were studied in an epithelial cell line of renal origin (LLC-PK1 cells). The oxalate uptake into the cells exhibited a marked sensitivity to extracellular, pH, in the present results with acidic pH stimulating and alkaline pH inhibiting the DIDS sensitive uptakes. The uptake of oxalate was clearly inhibited by DIDS, proportionally to the concentrations from 10 microM to 1 mM. Furosemide, chlorothiazide, probenecid and acetazolamide inhibited the oxalate uptake significantly. Probenecid has the most potency on the inhibition of the uptake in high concentrations, and acetazolamide needed a high concentration for the small effect. However, allopurinol has no effect on the uptake as well as dicarboxylates (malate, succinate and phenyl succinate) and organic acids (urate and para-amino hippurate). We discussed the mechanisms of the inhibition against the oxalate uptake concerning with each drug. It was suggested that probenecid may inhibit the oxalate carriers directly, while furosemide, chlorothiazide and acetazolamide may inhibit then by the direct actions and some secondary effects which are provided by those drugs.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1982

Calcium oxalate microcrystalline-associated arthritis in end-stage renal disease.

Chronic renal failure is known to be associated with secondary hyperoxalemia and the deposition of calcium oxalate in visceral organs, bones, and cartilage. We report the identification of calcium oxalate crystals in the synovial fluid of three patients with chronic renal failure. In one patient, calcium oxalate crystals were also identified within synovium and cartilage. Crystals were pleomorphic and bipyramidal. Some crystals were rod-like and had positive birefringence, thus tending to be confused with calcium pyrophosphate dihydrate when observed with only compensated polarized light microscopy. In one patients asymptomatic effusions were associated with joint capsule calcification, but otherwise normal knee radiographs. The other two patients had bilateral knee pain, one having coexistent features of osteoarthritis and the other chondrocalcinosis. Samples of proliferative synovium, joint capsule, and cartilage from the patient with chondrocalcinosis showed abundant calcium oxalate crystals, and not calcium pyrophosphate dihydrate or calcium hydroxyapatite. Thus, radiographically typical chondrocalcinosis may be due to calcium oxalate. Joint disease in chronic renal failure may be associated with calcium oxalate as well as the previously recognized apatite deposition.

Aged↗