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PubMed1982

Factors affecting endogenous oxalate synthesis and its excretion in feces and urine in rats.

It has been observed that the feces as well as urine of rats fed diets supplemented with 3% glycine and 5.2% hydroxyproline contain unexpectedly high amounts of endogenously formed oxalate. That intestinal microorganisms do not synthesize significant amounts of oxalate was indicated by the findings that oral tetracycline had no effect on oxalate excretion and that germ-free rats excreted more oxalate than conventional rats. Since little intraperitoneally injected [14C] oxalate appeared in the feces, and rat intestinal mucosa homogenates were found to produce oxalate from a variety of precursors of which glyoxylic acid was far the most important, it is probable that the intestinal mucosa may be an important source of fecal oxalate observed in these studies. Ninety percent of weanling rats fed complete diets supplemented with glycine and hydroxyproline developed urinary stones in 38 days. It has been concluded that in the treatment of patients with histories of calcium oxalate urolithiasis, more concern than is commonly shown should be directed towards the feeding of diets high in precursors of endogenous oxalate synthesis.

Animals↗
PubMedDate not supplied

Oxalate crystal deposits in renal tubules and cystic changes in 5/6 nephrectomized and normal rats.

Although the mechanism responsible for the genesis of acquired renal cysts in hemodialysis patients has not been clearly defined, the authors suggested that obstruction of the nephron by deposition of oxalate crystals may be an important factor. The present study was undertaken to examine this possibility in an experimental setting. Ten 5/6 nephrectomized rats were given daily subcutaneous injections of 5 mg sodium oxalate and allowed free access to saccharin sweetened water containing 2 mg/ml sodium oxalate. Six other 5/6 nephrectomized rats were controls. In addition, eight healthy rats received 10 mg sodium oxalate for 30 days. The earlier appearance and severe degree of tubular dilatation in oxalate-treated 5/6 nephrectomized compared with untreated 5/6 nephrectomized rats and the presence of renal tubular dilatation with oxalate deposits in normal rats treated with oxalate sodium are likely to be due to tubular obstruction or stenosis caused by oxalate deposition. In conclusion, oxalate deposits in the renal tubules seem to be an important factor in the formation of acquired renal cysts in chronic renal failure.

Animals↗
PubMed1994

High-yield production of oxalic acid for metal leaching processes by Aspergillus niger.

The complex-forming compound oxalic acid can effectively solubilise metals such as aluminium, iron, lithium and manganese. In order to produce high amounts of oxalic acid for biohydrometallurgical processes, it was the aim of this work to optimise oxalic acid production by Aspergillus niger, a fungus well known for its ability to produce oxalic acid. A. niger excreted 427 mmol oxalic acid l-1 if it was cultivated in a pH-controlled (pH 6.0) fed-batch run in a 2-l stirred tank reactor. Sucrose and lactose permeate were suitable carbon sources for oxalic acid production. In sucrose medium, A. niger produced high amounts of gluconic and oxalic acids, whereas in lactose permeate medium only oxalic acid was produced. Cultivation in green syrup and molasses media lead to high yields of biomass, but low oxalic acid production (< 20 mmol l-1).

Aspergillus niger↗
PubMed1994

Effect of formate and oxalate on fluid reabsorption from the proximal convoluted tubule of the anaesthetized rat.

1. It has recently been suggested that both formate and oxalate may be involved in the reabsorption of chloride from the proximal convoluted tubule (PCT). Reabsorption is achieved via a mechanism coupling Na(+)-H+ exchange to Cl(-)-anion exchange thus facilitating net NaCl transport. This possible mechanism was investigated further by observing the effect of luminal addition of formate and oxalate on proximal tubule transport in anaesthetized rats, previously prepared for in vivo microperfusion. 2. Addition of formate (0.25 mmol l-1) to the luminal perfusate resulted in a significant stimulation of fluid reabsorptive rate. 3. Oxalate was found to have a concentration-dependent effect on fluid reabsorption. Luminal oxalate concentrations below 0.05 mmol l-1 stimulated fluid reabsorption, while an oxalate concentration of 0.5 mmol l-1 inhibited fluid reabsorption. 4. The presence of formate (0.25 mmol l-1) and oxalate (0.001 mmol l-1) in the same luminal perfusate stimulated fluid reabsorption from the proximal tubule lumen, but the effects of formate and oxalate were not additive. 5. The removal of bicarbonate from the luminal perfusate and its replacement with phosphate had no significant effect on fluid reabsorptive rate. An alteration in perfusate pH was also ineffective. Addition of oxalate at high and low pH failed to stimulate fluid reabsorption compared with pH-matched control perfusions. 6. The experimental data suggest the involvement of both formate and oxalate in the reabsorption of NaCl from the proximal tubule lumen, though their influence may not be exerted through the same mechanisms.

Absorption↗
PubMed1982

Oxalate transport by proximal tubule of the rabbit kidney.

Oxalate transport was examined in isolated perfused segments of the proximal tubule of the rabbit. When oxalate was present in a concentration of 10(-5) M in the bathing and perfusing solutions, there was a net secretory flux of oxalate of 36.4 +/- 1.4, 34.7 +/- 4.3, and 20.7 +/- 2.8 x 10(-15) mol . min-1 . mm-1 in the superficial S1, S2, and S3 segments, respectively, at a bath temperature of 37 degrees C. The net secretory flux of oxalate in the juxtamedullary S1 and S2 segments was 12.8 +/- 2.5 and 12.5 +/- 3.6 x 10(-15) mol . min-1 . mm-1, respectively. Cooling to 25 degrees C resulted in a significant decrease in the net flux of oxalate. When oxalate was present in the bathing solution only (10(-5) M), the bath-to-lumen flux of oxalate was not different from the net flux in the superficial and juxtamedullary S2 segments. These studies demonstrate that oxalate undergoes net secretion in the rabbit proximal tubule. This occurs against an electrical gradient, in the absence of concentration gradients, and can be inhibited by cooling, suggesting an active transport process. There is significant internephronal heterogeneity in the proximal tubule for oxalate secretion.

Animals↗
PubMed1988

Oxalate transport via the sulfate/HCO3 exchanger in rabbit renal basolateral membrane vesicles.

We evaluated the mechanism of oxalate transport in basolateral membrane vesicles isolated from the rabbit renal cortex. An outward HCO3- gradient induced the transient uphill accumulation of oxalate and sulfate, indicating the presence of oxalate/HCO3- exchange and sulfate/HCO3- exchange. For oxalate, sulfate, or 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid, the K1/2 value for oxalate/HCO3- exchange was nearly identical to that for sulfate/HCO3- exchange, suggesting that both exchange processes occur via the same transport system. This was further supported by the finding of sulfate/oxalate exchange. Thiosulfate/sulfate exchange and thiosulfate/oxalate exchange were also demonstrated, but a variety of other tested anions including Cl-, p-aminohippurate, and lactate did not exchange for sulfate or oxalate. Na+ did not affect sulfate or oxalate transport, indicating that neither anion undergoes Na+ co-transport or Na+-dependent anion exchange in these membrane vesicles. Finally, we found that the stoichiometry of exchange is 1 sulfate or oxalate per 2 HCO3-, or a thermodynamically equivalent process. We conclude that oxalate, but not other organic or inorganic anions of physiologic importance, can share the sulfate/HCO3- exchanger in renal basolateral membrane vesicles. In series with luminal membrane oxalate/Cl- (formate) exchange, exchange of oxalate for HCO3- or sulfate across the basolateral membrane provides a possible transcellular route for oxalate transport in the proximal tubule.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1983

Alterations in circadian rhythmicity in calcium oxalate renal stone formers.

The circadian (circannual for oxalic acid) variations of 13 urinary variables (volume, creatinine, calcium, oxalic acid, glycolic acid, 17-ketosteroids, 17-hydroxycorticosteroids, phosphates, urea, uric acid, chloride, sodium, and potassium) have been documented in 7 calcium oxalate renal stone formers and 7 healthy men (control group). Urine was collected every 4 h over a period of 24 h. All subjects had the same synchronization: diurnal activity from 07(00) to 23(00) +/- 1 h and nocturnal rest; meals were given at fixed clock hours (08(00), 12(30) and 20(00) +/- 1 h). A statistically-significant rhythm (p less than 0.05) was validated for all variables except urea and calcium in healthy men. In renal stone formers, 6 variables (calcium, oxalic acid, and glycolic acid in particular) had no detectable circadian rhythm. However, a periodicity of c. 8 h (ultradian rhythm) was demonstrated for calcium and oxalic acid with peaks being located around 02(00), 10(00), and 18(00). No circannual variations in oxalic acid output could be observed. The present study shows an alteration of the periodicity of calcium and oxalic metabolisms, i.e. the loss of a circadian (24-h) rhythm and the occurrence of an ultradian rhythm of 8 h. The risk of calcium-oxalate crystallisation appears thus greater at 02(00), 10(00), and 18(00). Furthermore, any study dealing with oxalic acid excretion should state the season of urine collection when comparing renal stone formers and healthy subjects, as significant differences in oxaluria may appear during the summer months and not during the rest of the year.

Adult↗
PubMed1980

[Absorption of calcium by growing goats: effect of oxalates].

The influence of sodium oxalate and calcium oxalate upon calcium digestibility was studied in growing goats. Furthermore, and in the same animals, calcium absorption efficiency was estimated after performing duodenal fistula which allowed us to introduce calcium chloride or calcium oxalate and sodium oxalate, in order to avoid ruminal bacteria action upon the forementioned compounds. Finally, calcium absorption of an isolated intestine loop was studied in conscious goats with a Crocker Markowitz fistula, in the presence or absence of oxalate. The addition of sodium oxalate to the diet did not significantly decrease calcium absorption; but when calcium was given as oxalate, absorption was considerably lower. When calcium was introduced as calcium chloride through duodenal fistula, absorption was the same as when the substance was given in the diet. Calcium absorption drastically decreased when sodium oxalate was introduced directly into the duodenum, this fact is confirmed when calcium absorption is estimated in a jejunal loop, which shows that the differences found in relation to the effect of dietary sodium oxalate or directly introduced in duodenum are due to the substance destruction by ruminal bacteria.

Absorption↗
PubMed1980

The effect of seed crystals on calcium oxalate nucleation.

Equimolar concentrations of calcium chloride and potassium oxalate were precipitated by a rapid mixing technique. The precipitated calcium oxalate particles were repeatedly counted at 15 min with a Coulter counter until reproducible total particle count and particle distribution curves were obtained. These values were compared with those found after the addition of various seed crystals and 10 per cent urine to the system. Calcium oxalate seed crystals markedly enhanced the nucleation rate of calcium oxalate (1), although only an estimated 16 per cent acted as effective nucleators. The addition of sodium acid urate crystals resulted in a small decrease in the number of calcium oxalate particles precipitated and fewer than 0.1 per cent of the crystals acted as effective nuclei. Seeds of agglomerated hydroxyapatite crystals also produced a small decrease in the number of calcium oxalate particles and fewer than 1 per cent of the seeds functioned as nucleators. The addition of 10 per cent urine to the system greatly increased the number of calcium oxalate particles produced although we are uncertain whether the urine provided effective nuclei or prevented particle aggregation. Our data indicate that, in a rapidly mixed system, neither sodium acid urate nor hydroxyapatite crystals are effective nucleators for the precipitation of calcium oxalate. The occurrence of epitaxial growth of calcium oxalate on these substances in urinary stones is therefore called into question.

Calcium Chloride↗
PubMed1994

Tartrate dehydrogenase-oxalate complexes: formation of a stable analog of a reaction intermediate complex.

Oxalate has been shown to form a stable complex with Mn-tartrate dehydrogenase-NADH complexes which are proposed to mimic an intermediate formed during catalytic turnover. The formation of this complex can be detected under turnover conditions, where oxalate acts as a time-dependent inhibitor, and under equilibrium conditions, where oxalate binding triggers a slow protein conformation change detectable by fluorescence spectroscopy. Both the rate constant for the change in fluorescence intensity upon oxalate binding and the magnitude of the fluoresence change show a hyperbolic dependence on oxalate concentration. The time-dependent inhibition by oxalate is not consistent with a model in which oxalate binds to enzyme-NAD; rather, it is proposed that inhibition arises from binding to enzyme-NADH. The apparent dissociation constants of oxalate from enzyme-NAD+ and the enzyme-NADH complexes are 80 and 1 microM, respectively. The fluorescence changes which accompany oxalate binding are suggested to arise from a protein conformational change which serves to sequester reactants in the active site. Consistent with this hypothesis, it was observed that although some alternative pyridine nucleotide cofactors supported the multistep tartrate dehydrogenase-catalyzed net nonoxidative decarboxylation of meso-tartrate only at drastically reduced rates, none of the intermediate hydroxypyruvate was released into solution. In addition, fluorescence anisotropy measurements were conducted to investigate the mode of NADH binding.

Adenine Nucleotides↗
PubMed2000

Heated oyster shell with algal ingredient (AAACa) decreases urinary oxalate excretion.

In nine normal subjects, four men and five women between 23 and 49 years of age, 800mg calcium was orally administered as active absorbable algal calcium (AAA Ca) (A) and calcium carbonate (CaCO3) (B), to compare with non-calcium-containing placebo (C) in a crossover design. Calcium, oxalate, osmolality, creatinine, and pH were measured in the first three morning urine samples and Ca/osmolality, Ca/osmolality/body weight, Ca/creatinine, and oxalate/ osmolality were calculated to correct for urine dilution. Ca x oxalate product was also calculated, and Ca oxalate crystal in the sediment was microscopically examined, semiquantitatively estimated as -, +, ++, or , and numerically expressed as 0, 1, 2, or 3, respectively. Urinary Ca excretion was similar in groups A and B, but significantly larger than in group C, regardless of the method of correction for dilution. Urinary oxalate excretion with correction for osmolality, however, was significantly lower in A than in B and C, which gave similar values. Urine pH was similar among all three groups. Ca x oxalate product was significantly higher in C than in A, but A and B were not significantly different. AAA Ca appeared to decrease urinary oxalate excretion and Ca x oxalate product more efficiently than CaCO3, suggesting the possibility of inhibiting the formation of Ca x oxalate kidney stones.

Adult↗
PubMed1989

The determination of plasma oxalate concentrations using an enzyme/bioluminescent assay. 2. Co-immobilisation of bioluminescent enzymes and studies of in vitro oxalogenesis.

An inexpensive, continuous flow assay for the determination of oxalate in plasma is described. The assay is based on the bioluminescent determination of NADH, a product of the degradation of oxalate by oxalate decarboxylase and formate dehydrogenase, using bioluminescent enzymes immobilized on cyanogen bromide-activated sepharose. The detection limit of the assay is 0.8 mumol/l. Intra-batch CV values of 5.2 and 3.8% were obtained at oxalate concentrations of 18 and 60 mumol/l. Recovery of added oxalate averaged 100.7%. Plasma oxalate ranged from less than 0.8 to 2 mumol/l in 14 healthy subjects, and from 6 to 134 mumol/l in 125 patients with renal disease treated by continuous ambulatory peritoneal dialysis. Ascorbic and dehydroascorbic acid did not directly interfere in the assay. In vitro oxalogenesis was observed in blood from 12 healthy subjects, but only after samples had stood at room temperature for more than 6 h. No significant oxalate generation occurred in blood from 24 patients with impaired renal function, even after standing at room temperature for 24 h. Oxalate generation was inhibited by the addition of oxalate to plasma, but the addition of urea and creatinine was without effect.

Creatinine↗
PubMed1989

The quantitation of oxalate in amniotic fluid by ion-chromatography.

Calcium oxalate is the predominant constituent of most kidney stones. The rare genetic disorder, primary hyperoxaluria, is characterized by the continuous excessive synthesis and urinary excretion of oxalic acid, leading to stone formation and renal insufficiency. The earliest measurement of oxalate in suspected cases of primary hyperoxaluria is advantageous and would lend support for continued analysis and eventual confirmation of the disease. Therefore, we quantitated oxalate levels in amniotic fluid (AF) using medium pressure ion-exchange chromatography. The mean concentration of oxalate in amniotic fluid was 1.67 mg/l +/- 0.8 (SD); (range 0.64 to 5.11 mg/l). The mean oxalate/creatinine ratio (O/C) was 0.23 +/- 0.11 (SD); (range 0.07 to 0.53). This ratio is similar to that found in the urine of infants less than 1 year (0.19 +/- 0.10; n = 17). There was no significant difference between males and females in oxalate concentration or O/C ratio. Regression analysis showed no significant correlation of fetal age with oxalate, O/C or creatinine. Studies in 13 sets of di-amnionic twins showed no statistical difference in oxalate or O/C between twin A and B. This study demonstrates the ability to accurately quantitate oxalate in amniotic fluid by ion-chromatography, and suggests that this may have a potential application in the initial screening process for the prenatal detection of primary hyperoxaluria.

Amniotic Fluid↗
PubMed2004

Idiopathic calcium oxalate urolithiasis: risk factors and conservative treatment.

Idiopathic calcium oxalate urolithiasis is a frequent and recurrent multifactorial disease. This review focuses on urinary and dietary risk factors for this disease and conservative strategies for rectifying them. Dietary oxalate and calcium and their respective urinary excretions have been extensively investigated during the last 10 years. Urinary oxalate has emerged as the most important determinant of calcium oxalate crystallization while the role of urinary calcium has shifted to bone balance and osteoporosis. Dietary calcium restriction increases urinary oxalate and contributes to a negative bone balance. It has therefore been abandoned as a means to reduce the risk of calcium oxalate kidney stone formation. Calcium oxalate kidney stone patients are advised to increase their fluid intake to achieve a urine volume of 2 l or more; the recommended calcium intake is 800-1200 mg/day; high oxalate foods should be restricted; daily protein intake should be between 0.8 and 1 g/kg body weight/day; essential fats should be included; vegetable and fruit (except oxalate-rich vegetables) intake should be increased. The use of calcium supplements has potential benefits but needs to be examined further.

Animals↗
PubMed1997

Urinary oxalate excretion and its role in vulvar pain syndrome.

OBJECTIVE: This study was undertaken to determine the urinary oxalate excretion patterns in patients with vulvodynia compared with controls and to evaluate antioxalate therapy in women with vulvar pain syndrome (vulvodynia). STUDY DESIGN: A total of 130 consecutive patients with vulvar pain syndrome and 23 volunteers without symptoms collected urine specimens for 24 hours; each voiding was saved in individual labeled containers and refrigerated. The specimens were analyzed individually for oxalate and calculated according to 24-hour concentration, volume, and peak oxalate by hour. A total of 59 patients were treated with low-oxalate diets and calcium citrate for 3 months and evaluated for objective relief of vulvar pain. RESULTS: The 24-hour excretion of oxalate was almost identical in controls and vulvodynia patients. The total 24-hour excretion was directly proportional to the volume of urine excreted (p < 0.001). No significant differences were found in peak oxalate excretion (95% confidence intervals). The number of voidings was higher in the vulvodynia cohort (p < 0.02). The 59 women with elevated oxalate concentrations (> 1 mg/40 dl) were treated with an antioxalate regimen. Fourteen (24%) demonstrated an objective response, but only 6 (10%) could have pain-free sexual intercourse. CONCLUSIONS: Urinary oxalates may be nonspecific irritants that aggravate vulvodynia; however, the role of oxalates as instigators is doubtful.

Circadian Rhythm↗
PubMed1976

Oxalate, calcium uptake and ATPase activity of sarcoplasmic reticulum vesicles.

Ca++-uptake and Mg++-Ca++-dependent ATPase activity of skeletal muscle sarcoplasmic reticulum vesicles were reciprocally affected by increasing the oxalate concentration from 0 to 4 mM. At 0-0.1 mM oxalate approximately 17% of the calcium was removed by the vesicles from the medium while the ATPase activity was maximal (approximately 0.66 mumoles Pi mg-1 protein min-1). Between 0.1 to 0.2 mM oxalate the ATPase activity was reduced to one-fifth but the uptake rose sharply and 100% of the 45Ca++ was removed from the medium. The uptake was maintained at this level at oxalate concentrations greater than 0.4 mM but the ATPase activity remained inhibited. The kinetics of Ca++-uptake and ATPase activity were also differentially affected by oxalate. In the presence of oxalate, ruthenium red had only a very slight inhibitory effect on the calcium uptake. Addition of 0.1 mM EGTA removed 80% of the Ca++ from preloaded vesicles within 10 min. The formation of insoluble Ca-oxalate salt on the surface of the vesicle is suggested by these results. Calculations based on the Ksp of the calcium oxalate salt are presented to show its formation and the possible speciation of a Ca-oxalate complex which may affect the Ca++-uptake and ATPase activity.

Animals↗
PubMed1990

Absence of effect of allopurinol on oxalate excretion by stone patients on random and controlled diets.

After 1 year of allopurinol treatment in 36 patients with a history of uric acid and/or calcium oxalate lithiasis and hyperuricosuria, we observed that in addition to the desired decreases in uric acid there were apparently significant decreases in urinary oxalate levels: 37 +/- 3 mg. per day (mean +/- standard error) before therapy and 31 +/- 4 mg. per day after a mean decrease of 16% (p less than 0.05) with an equivalent decrease in the supersaturation (calcium oxalate) of the urine. However, the decrease in oxalate could have been related to changes in dietary habits rather than to any specific effects of allopurinol on oxalate metabolism. Therefore, we recruited 26 of the patients for a study in which dietary factors were controlled. Each participant was assigned to 1 of 3 diet groups: low or high protein, or a customary diet. Each patient collected a urine specimen while on allopurinol and again after the medication was discontinued. With analytical procedures that we ascertained to be free of any significant methodological bias, we observed no significant changes in urinary oxalate excretion that could be attributed to allopurinol. There were significant differences in oxalate excretion on versus off allopurinol between the low and high protein groups, with higher oxalate levels found for the latter group. Our results indicate that allopurinol does not have a specific effect on oxalate metabolism or oxaluria.

Adult↗
PubMed1986

Membrane interactions with calcium oxalate crystals: variation in hemolytic potentials with crystal morphology.

Crystal-induced membranolysis of human red blood cells has been quantitated for calcium oxalate monohydrate and calcium oxalate dihydrate crystals. Calcium oxalate monohydrate crystals are significantly more membranolytic than calcium oxalate dihydrate crystals at constant surface area. If the crystal morphology of calcium oxalate monohydrate is altered by grinding, the lytic potential at constant surface area is markedly reduced. However, altered calcium oxalate dihydrate crystals are as lytic as natural calcium oxalate dihydrate crystals at constant surface area. Differences in the calcium oxalate monohydrate and dihydrate crystal structures, specifically the structural characteristics of the disordered water channel in calcium oxalate dihydrate, can explain these different membranolytic characteristics.

Calcium Oxalate↗