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PubMed1995

Glucagon increases urinary oxalate excretion in the guinea pig.

Factors that influence hepatic oxalate synthesis are poorly defined. Hormones are important regulators of hepatic metabolism and could potentially be involved. The effects of hyperglucagonemia were examined in guinea pigs injected with either saline or pharmacological doses of glucagon for 4 days. Glucagon treatment increased mean urinary oxalate excretion by 77% in male and 34% in female animals. The levels of hepatic peroxisomal enzymes involved in oxalate synthesis declined with glucagon treatment, but experiments with isolated peroxisomes indicated that oxalate synthesis in vitro was unaffected. Glucagon decreased hepatic alanine levels by 66%, lactate by 69%, and pyruvate by 73%, but glycolate and glyoxylate levels were unaffected. This decrease in alanine would substantially lower the activity of alanine-to-glyoxylate aminotransferase activity in vivo and make more glyoxylate available for oxalate synthesis. The decrease in lactate and pyruvate concentrations would stimulate the enzymatic conversion of glyoxylate to oxalate and may account for the increase in oxalate synthesis without an increase in glyoxylate concentration. These results demonstrate that hepatic oxalate synthesis is influenced by metabolic changes and that alterations in hepatic alanine, lactate, and pyruvate concentrations may be important elements.

Animals↗
PubMed1996

Mechanisms of stimulation of proximal tubule chloride transport by formate and oxalate.

We have previously demonstrated that formate and oxalate stimulate volume absorption in the rat proximal tubule, consistent with Cl-/formate and Cl-/oxalate exchange process across the apical membrane. To sustain Cl- absorption by these processes requires mechanisms for recycling formate and oxalate from lumen to cell. The aims of the present study were to characterize these mechanisms of formate and oxalate recycling. Proximal tubules and peritubular capillaries were simultaneously microperfused in the rat kidney in situ. Serum formate concentration was determined to be 56.5 +/- 7.7 microM. Addition of 5, 50, and 500 microM formate to both luminal and capillary perfusates significantly increased net Cl- absorption (Jcl) by 26, 26, and 46%, respectively. Jcl was stimulated 38% by 1 microM oxalate added to the perfusates. Removal of sulfate completely prevented the stimulation of Jcl by 1 microM oxalate but had no effect on the stimulation of Jcl by formate. Luminal addition of the Na+/H+ exchange inhibitor ethylisopropylamiloride completely blocked the stimulation of Jcl by 50 microM formate but had no effect on stimulation by oxalate. We conclude that physiological concentrations of formate and oxalate markedly stimulate Cl- and fluid absorption in the rat proximal convoluted tubule. Whereas formate recycling most likely involves Na+/H+ exchange in parallel with H(+)-coupled formate entry, oxalate recycling involves sodium-sulfate cotransport in parallel with sulfate/oxalate exchange.

Amiloride↗
PubMed1998

Enhanced oxalate transport in nucleated red blood cells.

OBJECTIVE: This study was aimed to determine the presence of oxalate exchange/binding protein in the nucleated red blood cells (RBC). MATERIALS AND METHODS: Intact RBC, nuclei, RBC membrane, nuclear membrane and histones were isolated and 14C-oxalate exchange/binding was studied. RESULTS: The rate of oxalate anion exchange by nucleated erythrocytes was found to be higher (K = 1.24/min) than that of human RBC (K = 0.51/min) but less than that of nuclei (K = 1.55/min). Oxalate flux rate was pH- and temperature-dependent. Oxalate exchange was reduced by 35% for both chicken RBC and nuclei in presence of sulfate, bicarbonate, phosphate and succinate. Both plasma membrane and nuclear membrane showed maximal oxalate binding activity at pH 7.4, while in the nuclear basic protein fraction it was at pH 4.5. 4,4'-Diisothiocyanostilbene-2,2'-disulfonate, an anion transport inhibitor, inhibited the oxalate exchange and binding activity in both erythrocytes as well as nucleus. CONCLUSION: Nucleated RBC can be useful model system for studying the interaction of oxalate with nuclear components.

Animals↗
PubMed1998

Study of calcium oxalate crystalluria on renal and vesical urines in stone formers and normal subjects.

OBJECTIVE: The aim of this study is to compare vesical and renal calcium oxalate crystalluria in an attempt to correlate crystal formation with chemical composition and calcium oxalate saturation of renal urine. MATERIAL AND METHODS: Urine specimens were directly collected from the bladder and the kidney, of 11 stone formers and 11 control subjects under general anesthesia. The type of crystals present in urine as well as their size, number by cubic millimeter and state of aggregation were determined. In addition, calcium, magnesium, sodium, chloride, phosphate, citrate, oxalate, pyrophosphate and uric acid were measured in order to evaluate the calcium saturation status (EQUIL V program). RESULTS: Calcium oxalate crystals were detected in 3 stone formers (27%) and 2 control subjects (18%) in vesical urine and in 4 stone formers (36%) and 3 control subjects (27%) in renal urine. Only 2 stone formers presented with simultaneous renal and vesical crystalluria. Subjects of the two groups with and without renal crystalluria were compared in terms of chemical composition and calcium oxalate saturation of renal urine. Crystalluric subjects (n = 7) had significantly higher uricosuria (p = 0.02), calciuria (p = 0.04), magnesiuria (p = 0.04) and calcium oxalate molar product (p = 0.05) than noncrystalluric (n = 15); calcium oxalate saturation was similar (p = 0.5). CONCLUSIONS: Beyond theorical considerations on lithogenesis, our observations and in particular the apparent discrepancy between renal and vesical crystalluria pose the problem of the clinical interest of the evaluation of calcium oxalate crystalluria based on freshly voided urine in the assessing the lithogenic risk or in the follow-up of patients who are particularly prone to stone recurrence.

Adult↗
PubMed2004

Microorganisms and calcium oxalate stone disease.

Microorganisms may have a role in the pathogenesis and prevention of kidney stones. The subjects of this review include nanobacteria, Oxalobacter formigenes, and lactic acid bacteria. Not reviewed here is the well-described role of infections of the urinary tract with Proteus species and other urease-producing organisms associated with struvite stone formation. Nanobacteria have been proposed to be very small (0.08-0.5 nm), ubiquitous organisms that could play a role in stone formation. The theory is that nanobacteria can nucleate carbonate apatite on their surfaces and thereby provide the nidus for stone formation. However, their existence remains uncertain and many investigators are openly skeptical. Recent investigations suggest that they are artifacts, and not actually living organisms, but their proponents continue to study them. O. formigenes is an obligate anaerobe which may be important in the prevention of stone formation. Its sole substrate for generation of ATP is oxalate. It may thereby metabolize its human host's dietary oxalate and diminish intestinal absorption and subsequent urinary excretion of oxalate. There is evidence that the organism's absence, perhaps sometimes due to courses of antibiotics, may be a cause of hyperoxaluria and stone formation. In early investigations, patients not colonized with the organism can be recolonized. Urinary oxalate can be diminished by accompanying an oxalate-containing meal with the organism. One study demonstrated that a preparation of lactic acid bacteria successfully reduced urinary oxalate excretion in 6 patients with calcium oxalate stones and hyperoxaluria. The mechanism of this effect is uncertain since these bacteria lacked the gene possessed by O. formigenes which codes for that organism's oxalate uptake mechanism. The author is currently completing a small randomized controlled clinical trial with this preparation in calcium stone-forming patients with idiopathic hyperoxaluria.

Animals↗
PubMed1989

Acquired renal cysts in five-sixths nephrectomized rats: the roles of oxalate deposits in renal tubules and a renotropic factor.

The present study was undertaken to see if the oxalate deposits seen in renal tubules are a causative factor in the development of acquired renal cysts in chronic renal failure. Thirty 5/6 nephrectomized rats had free access to water containing 8 mg/ml of vitamin C (oxalate precursor) and 20 5/6 nephrectomized rats were given tap water without vitamin C. Oxalate deposits were found on microscopy in the renal tubules of vitamin C-treated rats in the 11th and 12th postnephrectomy months; however, acquired renal cysts were noted far in advance of the appearance of oxalate crystals. It has been suggested that the tubular dilatation seen in 5/6 nephrectomized rats is caused by an abrupt decrease in the functioning renal mass, leading to the production of a so-called 'renotropic factor'. However, oxalate deposits and renal tubular dilatation in oxalate-treated 5/6 nephrectomized rats preceded the renal tubular dilatation of untreated partially nephrectomized rats. In addition, these histological changes in the kidney were also seen in healthy rats which were given oxalate orally and subcutaneously. The present study suggested that the pathogenesis of acquired renal cysts is multifactorial. Renotropic factor may play an important role leading to nephron hyperplasia, but oxalate deposits in the renal tubules seem to be an important factor in the formation of these cysts.

Animals↗
PubMed1991

Investigations into the effect of glyoxylate decarboxylation and transamination on oxalate formation in the rat.

The decarboxylation and transamination reactions of glyoxylate, which divert this precursor from oxalate formation, have been investigated. Decarboxylation of glyoxylate is synergistic with 2-oxoglutarate and catalysed by 2-oxoglutarate:glyoxylate carboligase which co-chromatographs with the 2-oxoglutarate dehydrogenase complex. The activity is located in the mitochondrial fraction and is probably due to the E1 subunit of the complex. A greater amount of decarboxylation occurs from 2-oxoglutarate than from glyoxylate but the presence of 2-oxoglutarate does not affect oxalate formation from glyoxylate. There is no oxalate formation from 2-oxoglutarate. Studies with rat liver homogenates showed that a number of amino acids can participate in glyoxylate transamination. However, using isolated rat hepatocytes, these reactions did not have a significant effect on oxalate formation from glyoxylate with the exception of cysteine which caused an 80% reduction in oxalate formation. Investigation of this inhibition indicated that it was most likely due to the formation of a cysteine-glyoxylate adduct which makes glyoxylate unavailable for oxidation to oxalate. This cysteine inhibition of oxalate formation was also demonstrated in normal rats and rats made hyperoxaluric by injecting them with either glyoxylate or glycolate. The results indicate that sulphydryl compounds, which can have a therapeutic role as oxalate-lowering agents, may be able to be developed.

Aldehyde-Ketone Transferases↗
PubMed1991

The determination of oxalate in urine and plasma by high performance liquid chromatography.

We describe a simple, sensitive assay for oxalate in urine or plasma. Acidified urine is pretreated by dilution with neutral phosphate buffer and passage through a C18 cartridge. Stabilized plasma is diluted with neutral acetate buffer and oxalate extracted using a strong anion exchange cartridge. Treated samples are applied to an ion-paired chromatographic system and oxalate detected electrochemically. Recovery of oxalate from augmented samples exceeded 97% from both urine and plasma. Within- and between-assay coefficients of variation assessed at three concentrations were, respectively, better than 4.1% and 8.4% for urine and 3.9% and 5.2% for plasma. The reference range for urinary oxalate excretion is 109-497 mumols/24 h. The range for plasma oxalate concentration is 0.6-2.8 mumols/L or 0.7-3.9 mumols/L after an overnight fast or without dietary restriction, respectively. Urine and plasma oxalate concentrations from this method, gave correlation coefficients (r) of 0.97 and 0.98, respectively, when compared with those from established oxalate oxidase based assays.

Chromatography, High Pressure Liquid↗
PubMedDate not supplied

Urinary oxalate excretion increases in home parenteral nutrition patients on a higher intravenous ascorbic acid dose.

BACKGROUND: Vitamin C can be metabolized to oxalate. Case reports have suggested an association between IV vitamin C and urinary oxalate excretion. Recently, the US Food and Drug Administration required the dose of vitamin C in IV multivitamin preparations to be increased from 100 mg to 200 mg/d. We compared the urinary oxalate excretion level in stable home total parenteral nutrition (TPN) patients receiving both doses of vitamin C. METHODS: Each participant provided a 24-hour urine sample for oxalate determination on the vitamin C dose (100 mg/d), and again after at least 1 month on the increased vitamin C dose (200 mg/d). A 2-day diet diary was completed covering the day before and the day of the urine collection and was analyzed for oxalate and vitamin C content. Comparisons were made using Student paired t test and Wilcoxon signed rank. RESULTS: Thirteen patients (7 males/6 females) aged 63.1 +/- 12.2 years who had no history of nephrolithiasis and had received TPN for 55.9 +/- 78.8 months were enrolled. The most common indication for TPN was short bowel syndrome (38.5%). Eight patients had an intact colon. Urinary oxalate excretion increased on the 200-mg vitamin C dose, from 0.34 +/- 0.13 to 0.44 +/- 0.17 mmol/d (mean increase = 0.10 mmol/d; p = .04; 95% confidence interval 0.004 to 0.19 mmol/d). Oral intake of vitamin C and oxalate did not differ between the 2 collection periods. CONCLUSIONS: In therapeutically used doses, IV vitamin C increases urinary oxalate excretion, potentially predisposing susceptible individuals to nephrolithiasis. This factor should be considered in patients receiving home TPN.

Adult↗
PubMed2003

Oxalate exposure promotes reinitiation of the DNA synthesis and apoptosis of HK-2 cells, a line of human renal epithelial cells.

Oxalate, a metabolic end product, is a major constituent of kidney stones. Previously, we and others have demonstrated that oxalate is toxic to renal epithelial cells. In the present study, we characterized oxalate-induced cell death in HK2 cells, a line of renal epithelial cells from the human kidney. For these studies, HK2 cells were exposed to oxalate for various time points. Cells were examined for nuclear morphology, DNA fragmentation, and expression of various apoptosis-related proteins. Apoptotic mode of cell death was also confirmed by TUNEL assay. Results from these studies revealed that oxalate exposure resulted in time-dependent increase in DNA fragmentation. Maximum DNA fragmentation was observed at 2-24 hours following oxalate exposure. Results from Western blot analysis demonstrated an increased expression of the FAS ligand. Taken together, these data reveal that oxalate-associated nephrotoxicity results from oxalate-induced apoptosis of renal epithelial cells.

Apoptosis↗
PubMed2004

Effect of dehydroepiandrosterone on oxalate metabolism in rats.

Urinary oxalate plays an important role in the formation of calcium oxalate stone, and endogenous oxalate metabolism mainly occurs in the liver. Since dehydroepiandrosterone (DHEA) is known to have an effect on hepatocellular proliferation and on some hepatic enzymes, we examined the influence of DHEA on the activity of hepatic oxalate-related enzymes and on urinary oxalate excretion in rats. Fourteen male rats were castrated and divided into two groups. The control group was fed a standard diet, while the other rats were fed a diet containing 0.5% DHEA. After 4 weeks, the liver weight and the urinary levels of oxalate, glycolate, and glycine were significantly higher in the DHEA-treated rats than in the controls, while body weight did not differ between the two groups. Hepatic alanine:glyoxylate aminotransferase and glyoxylate reductase showed significantly higher activity in the DHEA-treated rats than in the controls, while glycolate oxidase activity was significantly reduced. Treatment with DHEA induced hyperoxaluria along with hepatocyte proliferation. This hyperoxaluria was probably caused by hepatocyte proliferation, but it could not be explained simply by the changes of hepatic oxalate-related enzymes. Investigation of the modulation of peroxisomal enzymes by peroxisomal proliferators or inhibitors may provide further insights into hepatocyte oxalate metabolism.

Animals↗
PubMed1981

Oxalate metabolism in man studied during total parenteral nutrition.

The mean urinary excretion of oxalate was 325 micromol/24 h in six patients during total parenteral nutrition (TPN). The urinary excretion of oxalate was considered to be equal to the endogenous oxalate production. A 2-day load of the oxalate precursor glycine given to five patients did not influence the oxalate excretion in spite of increased serum glycine concentrations. A 3-day load of the oxalate precursor ascorbic acid given to four patients increased the oxalate excretion in all patients. In one patient TPN was prolonged for 20 days without any change in the amount of oxalate excreted.

Adult↗
PubMed1981

Oxalate metabolism after intestinal bypass operations.

Hyperoxaluria and kidney stones are frequent following intestinal bypass operations. The urinary oxalate excretion was studied for 10-13 days during enteral and parenteral nutrition in six patients operated on because of massive obesity with a jejunoileostomy. The oxalate excretion in urine was higher than normal in all patients on normal diet. The excretion decreased on low-oxalate diet. Further decrease was observed during total parenteral nutrition (TPN). The oxalate excretion was stabilized at a low level within 48 h after the start of TPN and was unchanged during the rest of the study. This included a period of 2 days when a load of the oxalate precursor glycine (10 and 20 g) was given parenterally to five patients, resulting in increased serum glycine concentration. A slight decrease in oxalate excretion was found when the amino acid part (Vamin with 10% glucose) of the TPN solution was given enterally instead of parenterally in two patients. This study has indicated that the main reason for hyperoxaluria in patients with intestinal bypass operations is hyperabsorption of dietary oxalate. It seems likely that these patients have a normal endogenous oxalate production.

Adult↗
PubMed1990

The role of hyperoxaluria in the formation of calcium oxalate urinary calculi, and its association with other biochemical measurements.

The part played by hyperoxaluria in the formation of calcium oxalate urinary calculi was studied in 153 patients who had each been diagnosed as having calcium oxalate urinary calculi on one or more occasions. Seventy-seven of the patients excreted normal amounts of calcium (less than 6.2 mmol/d), and 76 had hypercalciuria (excretion greater than or equal to 6.2 mmol/d); each group was divided into a further two groups depending on whether the oxalate concentration was above or below 0.16 mmol/l. Pure calcium oxalate stones were more common in patients whose calcium excretion was normal, and mixed calcium oxalate and phosphate stones were more common among hypercalciuric patients. Urinary concentrations/day of magnesium, citrate, and phosphorus were significantly lower in the two groups in which the oxalate concentrations were below 0.16 mmol/l than in a normal control group, and magnesium and phosphorus were significantly lower in the two groups in which oxalate concentrations were less than 0.16 mmol/l than in the two in which they were above that value. The concentration of citrate was also lower, but not significantly so. In addition, the pH of the urine in patients with mixed stones was significantly higher in all groups than when the stones were composed of pure calcium oxalate.

Calcium Oxalate↗
PubMed1999

Aspects of calcium oxalate crystallization: theory, in vitro studies, and in vivo implementation.

There are three main approaches to urolithiasis research: theory, basic science, and clinical implementation. Although each approach has yielded meaningful results, there does not appear to be complete synergy between them. This article examines these approaches as they pertain to urinary calcium oxalate crystallization processes. Theoretical calculations were performed to examine the role of oxalate concentration on calcium oxalate supersaturation. The effects of magnesium, citrate, and combinations thereof on calcium oxalate crystallization kinetics were examined in a mixed suspension, mixed product removal crystallizer. Finally, male volunteers were given supplements of calcium alone and binary combinations of calcium, magnesium, and citrate to investigate their effects on the urinary supersaturation of calcium oxalate. Calculations showed that oxalate is 23 times more potent than calcium in its effect on the supersaturation of calcium oxalate. In the in vitro experiments, magnesium and citrate reduced the growth and nucleation kinetics as well as the supersaturation. In combination, these two components were more effective than the individual components in reducing the growth rate and the supersaturation. All of the supplements favorably altered the kinetic and thermodynamic risk factors. Calcium was the most effective in reducing the urinary excretion of oxalate. Articulation of these three approaches is essential for the meaningful investigation and understanding of urolithiasis.

Calcium Oxalate↗
PubMed1999

Role of sex hormones in experimental calcium oxalate nephrolithiasis.

It is unclear why men have a higher incidence of calcium oxalate nephrolithiasis than women. This study examined the role of sex hormones on urinary oxalate excretion and kidney stone formation in an experimental model of urolithiasis. Adult male and female Sprague Dawley rats with different sex hormone modulations were given 0.75% ethylene glycol for 2 wk to induce hyperoxaluria and kidney calcium oxalate crystal deposition. The study groups were: intact male and female rats; castrated male and female rats; intact male or female rats with opposite sex hormone implants; and castrated male and female rats with either testosterone or estradiol implants. Overall, a significant negative correlation between urinary oxalate and plasma estradiol/testosterone ratio was found. None of the estradiol-implanted rats, whether male or female, intact or castrated, developed kidney crystal deposits. The three groups of testosterone-implanted rats had a 43 to 88% rate of kidney calcium oxalate crystal deposition. These results indicate that androgens increase and estrogens decrease urinary oxalate excretion, plasma oxalate concentration, and kidney calcium oxalate crystal deposition. These findings may partly explain why nephrolithiasis is a predominantly male disease.

Animals↗
PubMed2000

Effect of renal ischaemia reperfusion on calcium oxalate retention.

The effect of ischaemia reperfusion induced renal injury for calcium oxalate deposition under normal and simulated conditions was studied. Male Wistar rats of both control (group I) and urolithic (group II) groups underwent (1 h) unilateral renal artery occlusion and were subjected to 1, 3, 6, 12, 24 and 72 h reperfusion. The group I rats subjected to 1 h renal ischaemia followed by 3 and 6 h reperfusion had significant oxalate retention than that of sham operated controls. In group II, under hyperoxaluric condition, in addition to accumulation of oxalate, calcium oxalate deposits were also observed. The increased retention of calcium oxalate was attributed to increased oxalate binding protein activity, oxalate synthesizing enzymes lactate dehydrogenase and xanthine oxidase activities and accumulation of calcium. Our findings suggested that renal cellular injury produced by ischaemia reperfusion could accelerate calcium oxalate precipitation reaction.

Animals↗
PubMed2002

Soluble and insoluble oxalate content of mushrooms.

Six different cultivars of edible fungi were bought from a local supermarket in Uppsala, Sweden and three different cultivars of wild growing fungi were harvested from the forest adjoining the city. The edible portions of the raw fungi were then analysed for total and soluble oxalate content. A portion of each fungi was then cooked by first boiling in a small amount of water followed by frying in a small amount of butter. The total oxalate content of the raw, commercially grown mushrooms ranged from 58.9 to 104.1 mg/100 g DM while the values for the total oxalate content of the cooked mushrooms ranged from 48.9 to 124.6 mg/100 g DM. Apart from cultivars ostronskivling and piopino the cultivated mushrooms contained mostly insoluble oxalates. Mushrooms harvested from the forest contained only soluble oxalate with the levels ranging from 29.3 to 40.2 mg/100 g DM in the raw tissue. Cooking marginally lowered the soluble oxalate content of these mushrooms. The levels of soluble and insoluble oxalates of all the mushrooms analysed were low compared to other common oxalate-containing vegetables.

Agaricales↗