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PubMed1989

Oxalate is overestimated in alkaline urines collected during administration of bicarbonate with no specimen pH adjustment.

We compared measurements of daily urine oxalate excretion in urines collected at the prevailing urine pH with measurements of urine oxalate excretion in urines collected into 20 mL of 6 mol/L HCl. We studied eight healthy adults fed constant diets. Urines were collected during control conditions and, in each subject, during the administration of NaCl, KCl, NaHCO3, or KHCO3, 90 mmol/day. Daily urine oxalate excretion calculated for collections made in acid averaged 271 (SD 79) mumol/day and did not vary with any of the salt supplements. When urines were collected at ambient urine pH (average 5.94, SD 0.23) during control conditions, and during the administration of NaCl or KCl, urine oxalate excretion averaged 263 (SD 88) mumol/day, a value not different from that for collections in acid. However, when urine was collected with no pH adjustment during NaHCO3 or KHCO3 administration (average pH 6.90, SD 0.14), apparent urine oxalate excretion averaged 398 (SD 132) mumol/day, significantly (P less than 0.025) exceeding the mean observed when urines were collected in acid. Moreover, the percentage increase in apparent oxalate excretion increased with urinary pH. These observations reinforce recommendations that urine specimens for measurement of oxalate be collected in acid to avoid the increase in apparent oxalate content that occurs during collection of alkaline urines. This increase presumably results from the well-known in vitro nonenzymatic conversion of ascorbate to oxalate.

Adult↗
PubMed1979

Pharmacokinetic studies of oxalate in man.

The observation of the plasma concentrations after rapid intravenous administration of inulin and 14C-oxalate to six normal and one hyperoxaluric subjects allowed estimations of the half-life of elimination of oxalate (mean 91.7 min), volume of distribution of oxalate (mean = 32.5 liters), calculation of the miscible oxalate pool (mean 3.7 mg), of the plasma oxalate concentration (mean = 11.1 microgram per 100 ml), of the oxalate clearance (252 ml per min), and the determination of the oxalate turnover rate (0.027 mg per min). The 14C-oxalate/inulin clearance ratio was 2.44 implying an additional excretion mechanism apart from glomerular filtration. Inasmuch as 97.2 per cent of the administered tracer were recovered unchanged in urine, nonrenal loss of oxalate is not an appreciable factor. The data of one hyperoxaluric patient are compared with those of the healthy subjects.

Amino Acid Metabolism, Inborn Errors↗
PubMed1977

Excretion of 4-pyridoxic acid and oxalic acid in patients with urinary calculi.

Urinary excretion of 4-pyridoxic acid and oxalic acid was investigated in 75 patients with urinary calculi and in 50 normal subjects on regular diet. Mean excretion of 4-pyridoxic acid was 0.85 and 0.90 mg per day, respectively, and mean excretion of oxalic acid was 27.5 and 28.0 mg per day, respectively. Statistically there was no difference between the two groups in 4-pyridoxic acid excretion or in oxalic acid excretion. There was a weak positive correlation between the urinary excretion of 4-pyridoxic acid and oxalic acid. Patients who were on ascorbic acid supplementation during the urine collection period excreted increased amounts of oxalic acid. It was concluded from this investigation that most patients with urinary calculi had 4-pyridoxic acid excretion and oxalic acid excretion within normal limits. Low 4-pyridoxic acid values were not combined with high excretion values of oxalic acid, and the nutritional state of vitamin B6 in patients with urinary calculi was assumed to be satisfactory in order to control the endogenous oxalic acid production. The significance of high excretion values of 4-pyridoxic acid and oxalic acid is discussed.

Ascorbic Acid↗
PubMed1997

Potential for bilateral nephrectomy to reduce oxalate release after combined liver and kidney transplantation for primary hyperoxaluria type 1.

Primary hyperoxaluria type 1 (PH-1) is frequently associated with end stage renal failure due to urinary calculi, obstructive uropathy and interstitial deposits of calcium oxalate. The currently accepted treatment for PH-1 is liver transplantation to replace the deficient enzyme peroxisomal alanine glycoxylate aminotransferase (AGT) and a simultaneous renal transplant to restore renal function. The transplanted kidney may become significantly impaired or fail when systemic calcium oxalate is eliminated by renal excretion. The native kidneys are a major source of this oxalate. This study was undertaken to determine whether there is a difference in oxalate clearance following combined liver-kidney transplant in patients with PH-1 by comparing the effect of native kidney nephrectomy at the time of transplantation against leaving the native kidneys in situ. Regression analysis was used to compare daily urinary oxalate excretion corrected for body surface area. There was a significant reduction in urinary oxalate excretion (P < 0.05) in the patient who had undergone bilateral nephrectomy compared to the patient whose native kidneys remained in situ for the first 100 d following combined liver and kidney transplantation. No difference was observed in the serum oxalate levels between patients over the same period or in the renal function assessed by creatinine clearance corrected for body surface area. Total body oxalate load was not determined in this study. A larger study should be undertaken to examine the benefits of nephrectomy in reducing oxalate deposition in recently inserted allografts for patients with PH-1.

Adult↗
PubMed1998

Glyoxylate synthesis, and its modulation and influence on oxalate synthesis.

PURPOSE: We define the major pathways of hepatic oxalate synthesis in humans, examine the association with other metabolic pathways and identify ways that oxalate synthesis may be modified. In addition, we suggest what is required for further progress in this area. MATERIALS AND METHODS: We consolidated relevant data primarily from recently published literature, considered new pharmacological approaches to decrease oxalate synthesis, and formulated an overview of the regulation and modification of oxalate synthesis pathways. RESULTS: Experiments with animals, including humans, animal cells and in vitro preparations of cellular components, support the existence of a major metabolic pathway linking the amino acids serine, glycine and alanine. Oxalate synthesis is a minor, secondary reaction of a cascade of reactions termed the glyoxylate pathway, which has a prominent role in gluconeogenesis and ureagenesis. The enzymatic steps and effectors which regulate glyoxylate and oxalate synthesis are not well characterized. Pharmacological approaches can reduce oxalate synthesis by diminishing the glyoxylate pool and possibly modifying enzymatic reactions leading to glyoxylate synthesis. CONCLUSIONS: The individual steps associated with glyoxylate and oxalate synthesis can be identified. The glyoxylate pathway has a significant functional role in intermediary liver metabolism but the way it is regulated is uncertain. Oxalate synthesis can be modified by drugs, indicating that primary and idiopathic hyperoxaluria may respond to pharmacological intervention.

Animals↗
PubMed1996

Formation of hydrated calcium oxalates in the presence of poly-L-aspartic acid.

The effect of poly-L-aspartic acid (PA) on the crystal structure of calcium oxalate crystals grown after spontaneous nucleation was evaluated as a function of relative supersaturation and calcium:oxalate ratio in a buffered salt solution, with pH and ionic strength in the range of normal human urine. PA was used as a model for naturally occurring acidic urine proteins that have been shown to inhibit nucleation and growth of calcium oxalate crystals. The crystals grown were characterized by optical microscopy and X-ray powder diffraction. It was observed that calcium oxalate monohydrate was the preferred crystalline form in the absence of added PA, and it was the only crystalline form obtained at most conditions tested without PA. However, the presence of PA favored the formation of calcium oxalate dihydrate crystals, when present in adequate quantities. The quantity of PA required to affect this change in preferred crystal structure was increased at higher supersaturations and at lower calcium:oxalate ratios, exhibiting a non-linear dependence on both variables. PA was also shown to be a kinetic inhibitor of calcium oxalate dihydrate crystallization. Aspartic acid monomer was found to cause no change in the preferred structure of calcium oxalate monohydrate at mass concentrations well beyond those required with PA to obtain 100% calcium oxalate dihydrate, indicating the critical importance of the polymeric nature of PA for this effect on crystal structure.

Calcium Oxalate↗
PubMed1995

Effects of urinary macromolecules on the nucleation of calcium oxalate in idiopathic stone formers and healthy controls.

Urinary macromolecules have attracted great interest because of their possible role as both promoters and inhibitors of calcium oxalate (CaOx) crystallization and it remains unclear whether there is any difference, in their nucleating activity, between stone formers and controls. We selected 9 male idiopathic CaOx stone formers whose 24-h urines presented no evidence of common urinary stone risk factors such as hypercalciuria, hyperoxaluria, hyperuricosuria, hypocitraturia, hypomagnesiuria or low glycosaminoglycans excretion and 12 male controls (matched for age and body weight) whose 24-h urines did not differ from those of stone formers. The study of urinary CaOx nucleation was made in freshly voided overnight urines whose biochemical composition was almost identical in the two groups. In filtered (0.22 micron) and ultrafiltered (10 kDa) urine we performed an oxalate tolerance test to determine the permissible increment of oxalate, the oxalate level for nucleation and the permissible increment of CaOx relative supersaturation (CaOx RS). In filtered urine from stone formers the permissible increment of oxalate was lower than controls (30 +/- 10.2 vs. 46.7 +/- 9.7 mg/l, P = 0.001), the oxalate level for nucleation was lower (64.4 +/- 14.2 vs. 79.5 +/- 15.6 mg/l, P = 0.035) and the permissible increment of CaOx RS was also lower (9.71 +/- 2.59 vs. 13.39 +/- 3.62, P = 0.018). In ultrafiltered urine these differences disappeared because the removal of macromolecules in stone formers significantly enhanced the oxalate-tolerance values. The difference between the change of the oxalate permissible increment of filtered and ultrafiltered urine allowed a distinction to be made between stone formers and controls that was not feasible in other ways (7.6 +/- 5.3 vs. 3.3 +/- 5.9 mg/l, P < 0.0001). The study suggests that, in idiopathic CaOx stone formers free from common urinary risk factors of CaOx crystallization, there is an increased tendency for CaOx nucleation in urine, which is mediated by macromolecular components.

Adult↗
PubMed1986

Multiorgan crystal deposition following intravenous oxalate infusion in rat.

Deposition of calcium oxalate is responsible for the pathologic manifestations of oxalosis and may contribute to multiorgan dysfunction in uremia and to the progression of renal damage after renal failure is established. We have developed a rat model of oxalosis using a single intravenous injection of sodium oxalate, 0.3 mmol./kg. body weight, in rats. Polarized light microscopy and section freeze-dry autoradiography were used to identify 14C-oxalate within the renal parenchyma and in extrarenal organs. 14C-oxalate crystals under three mu in length were identified within one min. of injection in proximal tubule lumens. Section freeze-dry autoradiography showed occasional minute crystals within glomeruli, heart, lung and liver at one hr. In contrast to concentrative cellular uptake demonstrated in rat renal cortical slices in vitro, intracellular accumulation of 14C-oxalate could not be detected in vivo. Within the first 24 hr., renal oxalate retention reached a maximum of 25 +/- 4 per cent of the injected dose/gm. kidney compared to a maximum of only 7 +/- 3 per cent/gm. kidney after intraperitoneal administration. Although less than one per cent dose/gm. kidney remained after one week, crystal fragments were scattered throughout the cortex and medulla, often surrounded by foci of interstitial nephritis. The retention of crystals in kidney and other body organs following i.v. oxalate provides a model of oxalosis which stimulates pathophysiologic events in a variety of clinical situations characterized by transiently or persistently elevated serum oxalate.

Animals↗
PubMed2003

Structure and bonding in solution of dioxouranium(VI) oxalate complexes: isomers and intramolecular ligand exchange.

Structural isomers of [UO(2)(oxalate)(3)](4-), [UO(2)(oxalate)F(3)](3-), [UO(2)(oxalate)(2)F](3-), and [UO(2)(oxalate)(2)(H(2)O)](2-) have been studied by using EXAFS and quantum chemical ab initio methods. Theoretical structures and their relative energies were determined in the gas phase and in water using the CPCM model. The most stable isomers according to the quantum chemical calculations have geometries consistent with the EXAFS data, and the difference between measured and calculated bond distances is generally less than 0.05 A. The complex [UO(2)(oxalate)(3)](4-) contains two oxalate ligands forming five-membered chelate rings, while the third is bonded end-on to a single carboxylate oxygen. The most stable isomer of the other two complexes also contains the same type of chelate-bonded oxalate ligands. The activation energy for ring opening in [UO(2)(oxalate)F(3)](3-), deltaU++ = 63 kJ/mol, is in fair agreement with the experimental activation enthalpy, deltaH++ = 45 +/- 5 kJ/mol, for different [UO(2)(picolinate)F(3)](2-) complexes, indicating similar ring-opening mechanisms. No direct experimental information is available on intramolecular exchange in [UO(3)(oxalate)(3)](4-). The theoretical results indicate that it takes place via the tris-chelated intermediate with an activation energy of deltaU++ = 38 kJ/mol; the other pathways involve multiple steps and have much higher activation energies. The geometries and energies of dioxouranium(VI) complexes in the gas phase and solvent models differ slightly, with differences in bond distance and energy of typically less than 0.06 A and 10 kJ/mol, respectively. However, there might be a significant difference in the distance between uranium and the leaving/entering group in the transition state, resulting in a systematic error when the gas-phase geometry is used to estimate the activation energy in solution. This systematic error is about 10 kJ/mol and tends to cancel when comparing different pathways.

Journal Article↗
PubMed1994

Acetylene Reduction by Symbiosomes and Free Bacteroids from Broad Bean (Vicia faba L.) Nodules (Role of Oxalate).

We report the presence of oxalate in the organic acid fraction of broad bean (Vicia faba L.) nodule cytosol. Using both high-performance liquid chromatography and enzymic assays, high levels of oxalate were detected (70.4 [plus or minus] 2.4 mM). To study the potential role of oxalate as an energy-yielding substrate for nitrogenase activity, free bacteroids were isolated from nodules and found to oxidize oxalate in support of C2H2 reduction under O2 tensions that were lower than those required to oxidize succinate, another dicarboxylate commonly detected in legume nodules. Symbiosomes of broad bean, isolated for the first time from amide-producing nodules, were provided with [14C]oxalate and found to have uptake kinetics with a lower affinity [Km(oxalate) = 330 [mu]M] than that for free bacteroids [Km(oxalate) = 130 [mu]M]. In anaerobic preparations of symbiosomes supplied with purified oxyleghemoglobin, O2 consumption was stimulated by oxalate from 20.2 [plus or minus] 0.8 nmol O2 min-1mg-1 protein to 24.5 [plus or minus] 1.1 nmol O2 min-1 mg-1 protein but always remained lower than the rate of O2 consumption in free bacteroids (32.2 [plus or minus] 1.4 nmol O2 min-1 mg-1 protein). Under these conditions, C2H2 reduction activity was 9.7 [plus or minus] 0.8 and 15.1 [plus or minus] 0.9 nmol C2H4 min-1 mg-1 protein for symbiosomes and bacteroids, respectively. These data support the suggestion that oxalate may play a role as a carbon substrate in support of N2 fixation in broad bean nodules.

Journal Article↗
PubMed1984

Substrate utilization by an oxalate-consuming spirillum species in relation to its growth in ozonated water.

The nutritional versatility of a vibrio-shaped, oxalate-utilizing isolate, strain NOX, obtained from tap water supplied with low concentrations of formate, glyoxylate, and oxalate, was determined by growth experiments with low-molecular-weight carbon compounds at high (grams per liter) and very low (micrograms per liter) concentrations. The organism, which was identified as a Spirillum species, appeared to be specialized in the utilization of a number of carboxylic acids. Yields of 2.9 x 10 CFU/mug of oxalate C and 1.2 x 10 CFU/mug of acetate C were obtained from growth experiments in tap water supplied with various low amounts of either oxalate or acetate. A substrate saturation constant of 0.64 muM oxalate was calculated for strain NOX from the relationship between growth rate and concentration of added oxalate. Maximum colony counts of strain NOX grown in ozonated water (dosages of 2.0 to 3.2 mg of O(3) per liter) were 15 to 20 times larger than the maximum colony counts of strain NOX grown in water before ozonation. Based on the nutritional requirements of strain NOX, it was concluded that carboxylic acids were produced by ozonation. Oxalate concentrations were calculated from the maximum colony counts of strain NOX grown in samples of ozonated water in which a non-oxalate-utilizing strain of Pseudomonas fluorescens had already reached maximum growth. The oxalate concentrations obtained by this procedure ranged from 130 to 220 mug of C/liter.

Journal Article↗
PubMed1998

Manganese Peroxidase-Dependent Oxidation of Glyoxylic and Oxalic Acids Synthesized by Ceriporiopsis subvermispora Produces Extracellular Hydrogen Peroxide.

The ligninolytic system of the basidiomycete Ceriporiopsis subvermispora is composed of manganese peroxidase (MnP) and laccase. In this work, the source of extracellular hydrogen peroxide required for MnP activity was investigated. Our attention was focused on the possibility that hydrogen peroxide might be generated by MnP itself through the oxidation of organic acids secreted by the fungus. Both oxalate and glyoxylate were found in the extracellular fluid of C. subvermispora cultures grown in chemically defined media, where MnP is also secreted. The in vivo oxidation of oxalate was measured; CO(2) evolution was monitored after addition of exogenous [C]oxalate to cultures at constant specific activity. In standard cultures, evolution of CO(2) from oxalate was maximal at day 6, although the MnP titers were highest at day 12, the oxalate concentration was maximal (2.5 mM) at day 10, and the glyoxylate concentration was maximal (0.24 mM) at day 5. However, in cultures containing low nitrogen levels, in which the pH is more stable, a better correlation between MnP titers and mineralization of oxalate was observed. Both MnP activity and oxidation of [C]oxalate were negligible in cultures lacking Mn(II). In vitro assays confirmed that Mn(II)-dependent oxidation of [C]oxalate by MnP occurs and that this reaction is stimulated by glyoxylate at the concentrations found in cultures. In addition, both organic acids supported phenol red oxidation by MnP without added hydrogen peroxide, and glyoxylate was more reactive than oxalate in this reaction. Based on these results, a model is proposed for the extracellular production of hydrogen peroxide by C. subvermispora.

Journal Article↗
PubMed1983

Production of oxalic acid by some fungi infected tubers.

Oxalic acid (as oxalate) was detected in four tubers commonly used for food in Nigeria-Dioscorea rotundata (White yam), Solanum tuberosum (Irish potato), Ipomoea batatas (Sweet potato), and Manihot esculenta (cassava). Whereas healthy I. batata had the highest oxalic acid content, healthy M. esculenta contained the lowest. When all tubers were artifically inoculated with four fungi-Penicillium oxalicum CURIE and THOM, Aspergillus niger VAN TIEGH, A. flavus and A. tamarii KITA, there was an increase in oxalate content/g of tuber tissue. The greatest amount of oxalate was produced by P. oxalicum in D. rotundata tuber. Consistently higher amounts of oxalate were produced by the four fungi in infected sweet potato tuber than in any other tuber and consistently lower amounts of oxalate were produced by the four fungi in Irish potato tuber. Differences in the carbohydrate type present in the tubers and in the biosynthesis pathway are thought to be responsible for variation in the production of oxalate in the different tubers by the four fungi used.

Fungi↗
PubMed1981

Effective therapy of enteric hyperoxaluria: in vitro binding of oxalate by anion-exchange resins and aluminum hydroxide.

Hyperabsorption of dietary oxalate is a major factor in the pathogenesis of enteric hyperoxaluria and a frequent complication of inflammatory bowel disease and ileojejunal bypass surgery. Successful treatment requires reduction in oxalate intake or inhibition of absorption of dietary oxalate by oral ingestion of oxalate binding agents. To identify such agents, oxalate binding by anion-exchange resins, gums, and aluminum hydroxide was measured under conditions that simulated those present in the intestinal lumen. Of the agents tested, those that bound oxalate best were colestipol and aluminum hydroxide. Strongly basic anion-exchange resins readily bound oxalate only in the absence of chloride. These results suggest that colestipol and aluminum hydroxide administration might reduce dietary oxalate absorption in patients with enteric hyperoxaluria.

Adsorption↗
PubMed1981

Localization of exogenous 14C-oxalate in rats determined by whole-body- and microautoradiography.

A single dose of 14C-oxalate was given to Wistar rats using a throat probe. The animals were sacrificed and the oxalate distribution was determined using whole-body-autoradiography. The results showed that a large portion of the absorbed oxalate had reached the bladder 30 min after administration. It is possible that this rapid renal excretion could lead to a short-term oxalate peak in the urine. The oxalate also showed a great affinity for bone. This suggests that there is a deep compartment for oxalate in bone. At the light microscopic level, the localization of 14C-oxalate in bone and in the gastric wall was demonstrated using microautoradiography. This appears to show that there is gastric excretion of absorbed oxalate. Further pharmacokinetic investigations are necessary to confirm this conclusion.

Animals↗
PubMed1984

Human plasma oxalate concentration re-examined.

In an attempt to reconcile estimates of plasma oxalate concentration by in vitro and in vivo assays, the in vitro radioenzymatic isotope dilution assay (REIDA) for plasma oxalate concentration was modified by initiating precipitation of calcium oxalate from plasma ultrafiltrates within one hour of phlebotomy. Plasma oxalate concentration form normal males was 4.0 mumol/1, consistent with reported values of 3.0 mumol/1 and 2.3 mumol/1 by enzymatic methods, and 2.8 mumol/1 by a gas chromatographic technique, and lower than 10.0 mumol/1 reported previously by chemical/enzymatic methods. This lower estimate of oxalate results, at least in part, from avoiding in vitro conversion of ultrafilterable substances to oxalate, and from the use of 'fire-cleaned' glassware. No difference in plasma oxalate was observed between age-matched, apparently healthy black and white males or with blood collected in the presence and absence of inhibitors of the conversion of glyoxalate to oxalate.

Adult↗
PubMed1985

The determination of plasma oxalate concentrations using an enzyme/bioluminescent assay.

An enzyme/bioluminescent assay for the determination of oxalate in plasma is described in which NADH, a reaction product of the enzymic degradation of oxalate by oxalate decarboxylase and formate dehydrogenase, is determined using a commercially available bioluminescent system. In contrast to most previously documented methods, this sensitive and specific assay requires minimal sample preparation allowing oxalate concentrations to be determined within 2 h of sample collection. The limit of detection for plasma samples is 0.8 mumol/l. The recovery of oxalate added to plasma averaged 99%. The inter-batch coefficient of variation, calculated by analysis of a plasma sample from a uraemic patient (oxalate concentration = 45.8 mumol/l) on 8 occasions, over a period of 5 wk, was 3.2%. Plasma oxalate concentrations in 35 normal subjects ranged from less than 0.8-1.5 mumol/l, which is in excellent agreement with values obtained by in vivo isotope dilution studies. Plasma oxalate was found to be strikingly elevated in a group of uraemic patients maintained on regular haemodialysis.

Adult↗
PubMed1981

Metabolic consequences of pyruvate kinase inhibition by oxalate in intact rat hepatocytes.

The effects of oxalate on glycolysis and glucose production from trioses were studied in hepatocytes isolated from fed and fasted rats. 1--In cells from fed rats oxalate inhibited glycolysis at the pyruvate kinase step, as shown by an increased phosphoenolpyruvate concentration, a decreased lactate and pyruvate production and a reduction of the glycolytic flux estimated by the rate of detritiation of [6-3H] glucose. The plot of 1/lactate production versus oxalate concentration showed that pyruvate kinase is a limiting step of glycolysis and allowed to determine the apparent inhibition constant for oxalate: about 3035 microM which is near the physiological concentration of blood oxalate. Under conditions where both pyruvate kinase and glycolytic flux are inhibited, oxalate had no effect on the synthesis of [14C] glucose from [14C] triose. 2--In hepatocytes prepared from fasted rats and incubated with lactate and pyruvate, oxalate decreased gluconeogenesis. In cells isolated from fasted rats and incubated with dihydroxyacetone, oxalate decreased lactate and pyruvate production whereas glucose synthesis remained unchanged. It is concluded that the inhibition of pyruvate kinase cannot by itself increase the gluconeogenic flux from triose.

Animals↗