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PubMed1989

Effect of animal and vegetable protein intake on oxalate excretion in idiopathic calcium stone disease.

Oxalate excretion was measured in healthy subjects and idiopathic calcium stone-formers on dietary regimens which differed in the type and amount of protein allowed; 24-h urine collections were obtained from 41 practising vegetarians and 40 normal persons on a free, mixed, "mediterranean" diet. Twenty idiopathic calcium stone-formers were also studied while on two low calcium, low oxalate diets which differed in that animal protein was high in one and restricted in the other. Vegetarians had higher urinary oxalate levels than controls and although the calcium levels were markedly lower, urinary saturation with calcium/oxalate was significantly higher. This mild hypercalciuria was interpreted as being secondary to both a higher intake and increased fractional intestinal absorption of oxalate. Changing calcium stone-formers from a high to a low animal protein intake produced a significant decrease in calcium excretion but there was no variation in urinary oxalate. As a result, the decrease in calcium oxalate saturation was only marginal and not significant. It was concluded that dietary animal protein has a minimal effect on oxalate excretion. Mild hyperoxaluria of idiopathic calcium stone disease is likely to be intestinal in origin. Calcium stone-formers should be advised to avoid an excess of animal protein but the risks of a vegetable-rich diet should also be borne in mind.

Adult↗
PubMed2005

Role of oxalic acid overexcretion in transformations of toxic metal minerals by Beauveria caledonica.

The fungus Beauveria caledonica was highly tolerant to toxic metals and solubilized cadmium, copper, lead, and zinc minerals, converting them into oxalates. This fungus was found to overexcrete organic acids with strong metal-chelating properties (oxalic and citric acids), suggesting that a ligand-promoted mechanism was the main mechanism of mineral dissolution. Our data also suggested that oxalic acid was the main mineral-transforming agent. Cadmium, copper, and zinc oxalates were precipitated by the fungus in the local environment and also in association with the mycelium. The presence of toxic metal minerals often led to the formation of mycelial cords, and in the presence of copper-containing minerals, these cords exhibited enhanced excretion of oxalic acid, which resulted in considerable encrustation of the cords by copper oxalate hydrate (moolooite). It was found that B. caledonica hyphae and cords were covered by a thick hydrated mucilaginous sheath which provided a microenvironment for chemical reactions, crystal deposition, and growth. Cryo-scanning electron microscopy revealed that mycogenic metal oxalates overgrew parental fungal hyphae, leaving a labyrinth of fungal tunnels within the newly formed mineral matter. X-ray absorption spectroscopy revealed that oxygen ligands played a major role in metal coordination within the fungal biomass during the accumulation of mobilized toxic metals by B. caledonica mycelium; these ligands were carboxylic groups in copper phosphate-containing medium and phosphate groups in pyromorphite-containing medium.

Biodegradation, Environmental↗
PubMed2000

Oxalate and calcium excretion in cystic fibrosis.

BACKGROUND: A patient with cystic fibrosis (CF) and repeated calcium oxalate renal stones prompted us to investigate other children for risk factors for this recognised complication of CF. METHODS: Twenty four hour urinary excretion of calcium, oxalate, and glycolate was measured in children with CF and no symptoms of renal tract stones. Normal diet and treatments were continued. RESULTS: In 26 children (aged 5-15.9 years) oxalate excretion was correlated with age; 14 of 26 children had oxalate excretion above an age appropriate normal range. There was a positive correlation between oxalate excretion and glycolate excretion. Mean calcium excretion was 0.06 mmol/kg/24 h with 21 of 24 children having calcium excretion below the normal range. CONCLUSIONS: Hyperoxaluria may reflect malabsorption although correlation between excretion of oxalate and glycolate suggests a portion of the excess oxalate is derived from metabolic processes. The hypocalciuria observed here may protect children with CF from renal stones.

Adolescent↗
PubMed1996

Assimilation of oxalate, acetate, and CO2 by Oxalobacter formigenes.

Oxalobacter formigenes is the only well-documented oxalate-degrading bacterium isolated from the gastrointestinal tract of animals. The production of ATP by Oxalobacter formigenes is centered around oxalate metabolism and oxalate is required for growth. A small amount of acetate (0.5 mM) is also required. Oxalate is decarboxylated to formate plus CO2 in nearly equimolar amounts. Experiments were conducted to determine which potential carbon sources (oxalate, acetate, formate, CO2) were assimilated by Oxalobacter formigenes and which metabolic pathways were operative in carbon assimilation. Measurements of the specific activities of total cell carbon after growth with different 14C-labeled precursors indicated that at least 54% of the total cell carbon was derived from oxalate and at least 7% was derived from acetate. Carbonate was also assimilated, but formate was not a significant source of cell carbon. Labeling patterns in amino acids from cells grown in [14C]oxalate or 14CO3 were different; however, in both cases 14C was widely distributed into most cellular amino acids. Carbon from [14C]acetate was less widely distributed and detected mainly in those amino acids known to be derived from alpha-ketoglutarate, oxaloacetate, and pyruvate. Cell-free extracts contained citrate synthase, isocitrate dehydrogenase, and malate dehydrogenase activities. The labeling observed in amino acids derived from acetate is in agreement with the function of these enzymes in biosynthesis and indicates that the majority of acetate carbon entered into amino acid biosynthesis via well-known pathways.

Acetates↗
PubMed1992

Effects of formate and oxalate on volume absorption in rat proximal tubule.

We examined the effects of formate and oxalate on the rate of fluid absorption (Jv) in the rat proximal convoluted tubule in situ. Proximal tubules were microperfused with a high-Cl-, low-HCO3- Ringer solution (pH 6.7), and the peritubular capillaries were perfused with a standard Ringer solution (pH 7.4), simulating conditions in the late proximal tubule. Jv, a measure of transtubular NaCl absorption under these conditions, was calculated from the change in luminal [3H]inulin. Addition of formate in the physiological range (500 microM) to the luminal perfusate increased Jv by 45%; addition of 500 microM formate to both luminal and capillary perfusates increased Jv by 57%. Similarly, addition of oxalate in the physiological range (5 microM) to the luminal perfusate increased Jv by 37%; addition of 5 microM oxalate to both luminal and capillary perfusates increased Jv by 57%. The stimulatory effects of formate and oxalate perfused in the lumen and capillaries were not additive. Addition of 4,4'-diisothiocyanostilbene-2,2'-disulfonate (DIDS, 0.1 mM) to the luminal perfusate had no effect on baseline Jv measured in the absence of added formate and oxalate but completely abolished the increment in Jv induced by formate and oxalate. Addition of the Cl(-)-channel blocker diphenylamine-2-carboxylate (DPC, 0.2 mM) to the capillary perfusate had no effect on baseline Jv but completely abolished the increment in Jv induced by formate and oxalate.(ABSTRACT TRUNCATED AT 250 WORDS)

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed2004

Expression of nuclear pore complex oxalate binding protein p62 in experimental hyperoxaluria.

Proteins are thought to play a major role in stone formation. Oxalate binding protein plays a vital role in the transport of oxalate. This study was aimed at determining whether hyperoxaluria induces the expression of nuclear pore complex oxalate binding protein p62 which has the transport function. Hyperoxaluria was induced in male Wistar rats by feeding 0.75% ethylene glycol in water. The oxalate binding activity of the nuclear pore complex protein increased markedly during experimental hyperoxaluria, whereas nuclear lamina had no binding at all. There was an alteration in the elution profile of the nuclear pore complex oxalate binding protein during the hyperoxaluric condition. The protein was purified and had a molecular weight of 62 kDa (data not shown). The purified protein showed cross-reactivity with the monoclonal antibody (MAb 414) and it showed homogeneity. The expression of this protein (p62) during the hyperoxaluric condition was determined by ELISA and a 3-fold increase was observed when compared to control rats. The increased expression is further confirmed by Western blotting and immunohistochemistry. The increase in p62 protein expression may be either due to increased expression of certain genes or degradation of the cell membrane by oxalate-induced cell injury. Thus, the present study suggests that the increased expression of this protein (p62) may be due to the oxalate induction.

Animals↗
PubMed1992

Clinical significance of phosphate in calcium oxalate renal stones.

We analysed calcium, magnesium, oxalate, citrate, urate and creatinine in urine and calculated risk factors in patients who had formed stones composed of calcium oxalate, and calcium phosphate, alone or as a mixture. Patients producing pure calcium oxalate stones (less than 0.1% phosphate) had a higher oxalate, and lower calcium excretion than stone-free subjects and patients forming other stone types. In contrast, patients producing calcium oxalate stones containing phosphate, even in trace amounts (greater than 0.1%) had no increase in oxalate excretion, but a higher calcium excretion than stone-free subjects. We could not correlate any computed variable (e.g. AP(CaOx) index) to stone composition. We conclude that pure CaOx stones may be the result of a high oxalate excretion, and that other calcium containing stones may have another and probably more complex aetiology, including primary precipitation of calcium phosphates.

Calcium Oxalate↗
PubMed1985

Oxidation of oxalate and polyamines by rat peroxisomes.

During renal failure, polyamines and oxalate levels are elevated in the serum and the glomerular filtrate and are dumped by the kidney. Both of these compounds can be catabolized by oxidative reactions. We have, therefore, investigated the intracellular distribution of oxalate oxidase and of a polyamine oxidase in normal female rat kidney and liver. Polyamine oxidase was demonstrable, using spermidine as substrate in the cerous peroxyhydrate procedure of Briggs et al., in peroxisomes of kidney tubule cells and of hepatocytes. Oxalate oxidase could not be studied with this technique due to precipitation of cerium oxalate in the incubation medium. To demonstrate oxalate oxidase, and to confirm the polyamine oxidase localization, we incubated aldehyde-fixed tissue in a diaminobenzidine medium at pH 8, following the approach of Veenhuis et al., in which oxidases are demonstrated by virtue of their production of H2O2, which then serves as a substrate for endogenous catalase. Using oxalate or spermidine as substrate with this approach, we found reaction product in typical renal peroxisomes; we also found reaction product, with the polyamine substrate, in hepatocyte peroxisomes. To strengthen the conclusion that the oxidases themselves are present in peroxisomes, we used a light microscopic method, based on the tetrazolium procedures of Allen and Beard to demonstrate polyamine and oxalate oxidase activities in bodies with the distribution of renal peroxisomes.

Animals↗
PubMedDate not supplied

Competition between oxalate and phosphate during active calcium accumulation by sarcoplasmic vesicles.

1. During ATP supported active calcium uptake oxalate as well as phosphate are accumulated with calcium. The uptake of calcium exceeds that of both anions by a small quantity--accounting for calcium binding to vesicular proteins and lipids. 2. From assay media containing phosphate and oxalate--nearly exclusively either oxalate or phosphate are taken up together with calcium by the sarcoplasmic reticulum vesicles. The mutual exclusion occurs in a very narrow concentration range of the anions. 3. In solutions containing phosphate and oxalate, calcium phosphate or calcium oxalate precipitates are formed according to their solubility properties. 4. When phosphate prevents oxalate from being taken up, calcium transport is inhibited. Inhibition occurs, because the concentration of ionized calcium inside the vesicles rises approximately 100-fold when oxalate is replaced by phosphate. The activity of the calcium dependent ATPase parallels the calcium uptake activity. 5. It is excluded that the inhibition of calcium uptake produced by phosphate is caused by an enhanced permeability of the sarcoplasmic reticulum membranes for calcium in the presence of phosphate.

Animals↗
PubMed2000

Patient and environmental factors associated with calcium oxalate urolithiasis in dogs.

OBJECTIVE: To test the hypothesis that breed, age, sex, body condition, and environment are risk factors for development of calcium oxalate uroliths in dogs. DESIGN: Case-control study. ANIMALS: 1,074 dogs that formed calcium oxalate uroliths and 1,724 control dogs that did not have uroliths. PROCEDURE: A validated multiple-choice questionnaire was designed to collect information from veterinarians and owners within 1 year of the date of urolith detection concerning signalment and environment of the dogs. Univariate and multivariate analyses were performed to calculate odds ratios to assess whether breed, age, sex, body condition, and environment were risk factors for calcium oxalate urolith formation. RESULTS: Middle-aged (8- to 12-year-old) castrated male dogs had increased risk for formation of calcium oxalate uroliths. Urolith formation was also associated with increasing age. Dogs of certain breeds, including Miniature and Standard Schnauzer, Lhasa Apso, Yorkshire Terrier, Bichon Frise, Shih Tzu, and Miniature and Toy Poodle, had increased risk for developing calcium oxalate uroliths. Overweight dogs also had increased risk. CONCLUSIONS AND CLINICAL RELEVANCE: Knowledge of patient and environmental risk factors for development of calcium oxalate uroliths may facilitate development of surveillance strategies that result in earlier detection of this disease. Modification of environmental factors and body weight may minimize calcium oxalate urolith formation and recurrence.

Age Factors↗
PubMed2003

Urinary saturation and risk factors for calcium oxalate stone disease based on spot and 24-hour urine specimens.

In 222 random spot urine specimens, the calcium concentration and calcium oxalate saturation [DG(CaOx)] were significantly higher among stone formers than among non-stone formers, while the citrate and creatinine-corrected citrate concentrations were lower. In 188 24-hour urine specimens, magnesium excretion was lower among stone formers than non-stone formers, while the creatinine-corrected calcium concentration and DG(CaOx) were higher. Among stone formers, there was no gender difference in the urinary concentrations of calcium, oxalate, citrate, magnesium, and DG(CaOx), but the creatinine-corrected calcium, citrate, and magnesium concentrations were higher in women, as well as 24-hour citrate excretion. The levels of calcium and oxalate have a major influence on DG(CaOx), while citrate and magnesium levels have a minor influence. DG(CaOx) was correlated with calcium and oxalate excretion, as well as with the creatinine-corrected calcium and oxalate concentrations. Approximately 5% of 24-hour urine specimens showed critical supersaturation, 80% showed metastable supersaturation, and 15% were unsaturated. Hypercalciuria or hyperoxaluria was fairly common (30% and 40%) in critically supersaturated urine, while it was less common (22.4% and 8.6%) in metastably supersaturated urine and was not detected in unsaturated urine. Hypocitraturia and/or hypomagnesiuria was more common (63.8-80%) at any saturation. The urinary calcium, oxalate, and citrate concentrations, as well as the creatinine-corrected calcium, oxalate, citrate, and magnesium concentrations and DG(CaOx), showed a significant correlation between 57 paired early morning spot urine and 24-hour urine specimens. The creatinine-corrected calcium and citrate concentrations of the early morning urine specimens were significantly correlated with the levels of calcium and citrate excretion in the paired 24-hour urine specimens. In conclusion, no parameter other than urinary saturation gives more than a vague indication of the risk of lithogenesis, so DG(CaOx) in either early morning urine or 24-hour urine specimens appears to be the best predictor of stone risk. Finally, the creatinine-corrected calcium and citrate concentrations in early morning urine can be used as a substitute for measuring 24-hour excretion.

Calcium Oxalate↗
PubMed1992

Idiopathic calcium oxalate nephrolithiasis: a cellular disease.

Physico-chemical, metabolic and hormonal theories regarding the pathogenesis of calcium oxalate nephrolithiasis do not sufficiently explain many features of this disease. The recent findings of an abnormally faster oxalate self-exchange and higher phosphorylation of band 3 in erythrocytes of idiopathic calcium oxalate stone formers suggest the hypothesis that nephrolithiasis may be a cellular disease, characterized by a defect in the function of the anion-exchange. The cellular anomaly seems genetically controlled. Band 3 anion exchanger function seems to be biochemically regulated through modulation of band 3 phosphorylation, which depends on cyclic AMP- and phospholipid-sensitive Ca2+ independent protein kinases. In this light, a reduced glycosaminoglycan concentration in the erythrocyte membranes of stone formers might play a role, as these molecules exert a strong inhibitory effects on band 3 phosphorylation and anion transport in vitro and in vivo. An in vivo trial was performed in which stone formers were administered glycosaminoglycans orally. A reduction in oxalate excretion, and oxalate renal clearance, and a simultaneous correction of the abnormal RBC oxalate flux and band 3 phosphorylation were observed. These data suggest the existence of a link between the erythrocyte abnormality and oxalate transport by the kidney and gut.

Animals↗
PubMed1990

Distribution of peroxisomes and glycolate metabolism in relation to calcium oxalate formation in Lemna minor L.

Calcium oxalate formation in Lemna minor L. occurs in structurally specialized cells called crystal idioblasts. Cytochemical and immunocytochemical protocols were employed to study the distribution of peroxisomes and the enzymes glycolate oxidase, glycine decarboxylase and ribulose 1,5-bisphosphate carboxylase-oxygenase (RuBisCO) in relation to synthesis of oxalate used for Ca oxalate formation. These enzymes are necessary for photorespiratory glycolate synthesis and metabolism. Using catalase cytochemistry, microbodies were found to exist in crystal idioblasts but were smaller and fewer than those found in mesophyll cells. Glycolate oxidase, which can oxidize glycolate to oxalate via glyoxylate, could not be found in microbodies of crystal idioblasts at any stage of development. This enzyme increased in amount in microbodies of mesophyll cells as they matured and could even be found in dense amorphous inclusions of mature cell peroxisomes. Glycine decarboxylase and RuBisCO could also be detected in increasing amount in mesophyll cells as they matured but could not be detected in idioblasts or were just detectable. Thus, Lemna idioblasts lack the machinery for synthesis of oxalate from glycolate. Based on these results and other available information, two general models for the generation and accumulation of oxalate used for Ca oxalate formation in crystal idioblasts are proposed. The biochemical specialization of crystal idioblasts indicated by this study is also discussed with respect to differentiation of cellular structure and function.

Alcohol Oxidoreductases↗
PubMed1990

The relation of clinical catastrophes, endogenous oxalate production, and urolithiasis.

A dose-related toxicity syndrome of renal, cerebral, and liver dysfunction; metabolic acidosis; and deposition of calcium oxalate crystals in tissues is reported in association with various apparently unrelated treatments for a wide range of diseases. The parenteral nutrient xylitol, the hyperosmolar agent glycerol, the polysorbate emulsifiers (e.g., in vitamin E preparations), the anesthetic methoxyflurane, and possibly the experimental hypoglycemic agent dichloroacetate all produce a toxicity syndrome very similar to that of ethylene glycol poisoning. In long-term, high-dose oral toxicity studies with rodents, these or similar agents also produce calcium oxalate bladder stones and bladder tumors. Studies with both unlabeled and labeled agents in humans and animals and in vitro experiments with purified enzymes, tissue homogenates, and isolated hepatocytes have provided both strong circumstantial and direct evidence for the existence of minor pathways of carbohydrate metabolism and of oxidative dealkylation and dehalogenation reactions in drug biotransformations that link these agents to endogenous oxalate production. Because urinary oxalate is now considered to be a critical factor in stone formation and because it is increasingly accepted that 80-90% of urinary oxalate is produced endogenously, it is now possible to formulate pathways that link oxalate production with dietary macronutrients. Therapeutic modifications of diet, in vivo hormonal milieu, and intracellular metabolic controls in relation to endogenous oxalate production may provide new forms of treatment for urolithiasis.

Animals↗
PubMed1989

Urinary oxalate excretion by very low birth weight infants receiving parenteral nutrition.

Renal calcifications have been described in very low birth weight (VLBW) infants, and diuretic drug-associated hypercalciuria is believed to play a role in the pathogenesis of this lesion. Hyperoxaluria is an important cause of renal stone formation in children and adults. Because parenteral nutrition solutions contain the oxalate precursors ascorbate and glycine, the relationship between total parenteral nutrition administration and oxalate excretion in VLBW infants was examined. Administration of approximately 0.5 g of total parenteral nutrition protein per kilogram per day to VLBW infants was associated with an increased urinary oxalate concentration and an increased urinary oxalate to creatinine ratio, when compared with VLBW infants receiving a glucose and electrolyte solution. A further increase in urinary oxalate concentration and oxalate to creatinine ratio was noted when total parenteral nutrition protein was increased to approximately 1.5 g of protein per kilogram per day. In VLBW infants who receive total parenteral nutrition, elevated urinary oxalate concentrations may develop and may be a factor in the pathogenesis of nephrocalcinosis in these infants.

Amino Acids↗
PubMed1989

Rapid enzymatic determination of urinary oxalate.

This new reagent kit for the quantitative measurement of oxalate in urine is a modification of an earlier Sigma oxalate assay procedure (procedure no. 590), a coupled enzyme assay involving oxalate oxidase and horseradish peroxidase. The new analytical procedure includes methods for processing urine specimens to eliminate interference with oxalate color development at 590 nm by ascorbic acid, divalent cations, and other urinary constituents. The reaction is complete in less than 5 min, and results are linearly related to oxalate concentration up to at least 1 mmol/L. Assay sensitivity and within-run and between-run precision were within the limits acceptable for other urinary oxalate procedures. Analytical recovery of added oxalate was close to 100%. This specific, simple, rapid procedure is suitable for routine clinical use.

Ascorbic Acid↗
PubMed1987

Effect of oxalate and malonate on red cell metabolism.

The addition of oxalate to blood stored in Citrate-phosphate-dextrose (CPD) produces a marked improvement in 2,3-diphosphoglycerate (2,3-DPG) preservation; an increase in 2,3-DPG levels can also be documented in short-term incubation studies. Oxalate is a potent in vitro inhibitor of red cell lactate dehydrogenase, monophosphoglycerate mutase, and pyruvate kinase (PK). In the presence of fructose 1,6-diphosphate the latter inhibitory effect is competitive with phospho(enol)pyruvate (PEP). Determination of the levels of intermediate compounds in red cells incubated with oxalate suggest the presence of inhibition at the PK step, indicating that this is the site of oxalate action. Apparent inhibition at the glyceraldehyde phosphate dehydrogenase step is apparently due to an increase in the NADH/NAD ratio. Oxalate had no effect on the in vivo viability of rabbit red cells stored in CPD preservatives for 21 days. Greater understanding of the toxicity of oxalate is required before it can be considered suitable as a component of preservative media, but appreciation of the mechanism by which it affects 2,3-DPG levels may be important in design of other blood additives. Malonate, the 3-carbon dicarboxylic acid analogue of oxalate late did not inhibit pyruvate kinase nor affect 2,3-DPG levels.

2,3-Diphosphoglycerate↗
PubMed1984

[Studies of influence of animal protein intake on the urinary risk factors of calcium oxalate stone formation].

To examine the effects of excessive animal protein intake on the urinary risk factors of calcium oxalate stone formation, protein loading experiments were performed on oxalate stone formers and normal subjects and rats. By animal protein loading of 61 g/day with diet which contained 400 mg of calcium and 46.6 mg of total oxalate, urinary calcium excretion increased by 27% both in stone formers and in normal subjects. Urinary oxalate excretion had a tendency to decrease on the 3rd and 4th days after loading. Urinary uric acid excretion increased significantly after loading. No significant change was recognized in the acid glycosaminoglycan (AGAG) and magnesium excretion. Urinary calcium excretion increased both in the high and low calcium diet groups after animal protein loading in the rat experiment. Urinary oxalate excretion increased after loading only in high oxalate low calcium diet group, therefore, it was supposed that animal protein intake caused increase of intestinal oxalate absorption.

Animals↗