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PubMed2003

Dietary risk factors for hyperoxaluria in calcium oxalate stone formers.

BACKGROUND: Hyperoxaluria is a major predisposing factor in calcium oxalate urolithiasis. The aim of the present study was to clarify the role of dietary oxalate in urinary oxalate excretion and to assess dietary risk factors for hyperoxaluria in calcium oxalate stone patients. METHODS: Dietary intakes of 186 calcium oxalate stone formers, 93 with hyperoxaluria (>or=0.5 mmol/day) and 93 with normal oxalate excretion (<0.4 mmol/day), were assessed by a 24-hour weighed dietary record. Each subject collected 24-hour urine during the completion of the food record. Oxalate content of foods was measured by a recently developed analytical method. RESULTS: The mean daily intakes of energy, total protein, fat and carbohydrates were similar in both groups. The diets of the patients with hyperoxaluria were estimated to contain 130 mg/day oxalate and 812 mg/day calcium as compared to 101 mg/day oxalate and 845 mg/day calcium among patients without hyperoxaluria. These differences were not significant. The mean daily intakes of water (in food and beverages), magnesium, potassium, dietary fiber and ascorbic acid were greater in patients with hyperoxaluria than in stone formers with normal oxalate excretion. Multiple logistic regression analysis revealed that urinary oxalate excretion was significantly associated with dietary ascorbate and fluid intake, and inversely related to calcium intake. Differences of estimated diet composition of both groups corresponded to differences in urinary parameters. CONCLUSIONS: These findings suggest that hyperoxaluria predominantly results from increased endogenous production and from intestinal hyperabsorption of oxalate, partly caused by an insufficient supply or low availability of calcium for complexation with oxalate in the intestinal lumen.

Adult↗
PubMed1992

Effect of calcium on oxalate uptake and transport by the rat intestine.

The effect of calcium concentration (0-10 mmol 1(-1)) on oxalate uptake and transport was investigated in vitro using everted gut segments and sacs. Increase in calcium concentration in the incubation medium led to an increase in the amounts of precipitated oxalate on the intestine; however, the net oxalate flux to the serosal side decreased. The ions, i.e. Ca2+, Ox2-, H2PO4-, HPO4(2-), present in the incubation medium favoured formation of hydroxyapatite and calcium oxalate crystals, as evidenced by Equil II analysis and free energy of the system. The nature of precipitates was confirmed by elemental analysis, X-ray diffraction spectrometry and electron microscopy. Oxalate precipitated on the intestine following incubation with calcium could be released into a calcium- and oxalate-free medium. Animals fed oxalate in the absence and presence of calcium revealed that, during 1 h in the absence of calcium, oxalate moved down the intestinal tract as a distinct peak of greater than 50% (70-90 cm in the intestine), leaving less than 10% in the stomach and first 50 cm of the intestine. In the case of animals fed calcium along with oxalate, 35% of the oxalate was still present in the stomach, and the amounts of oxalate in the intestinal segments gradually increased from 4.5% to 21.7% (0-90 cm) and dropped to 2.1% in the next 20 cm. Since oxalaemia and oxaluria appear to be influenced by intestinal oxalate absorption, the present observations may help to improve understanding of the pathophysiology of disorders exhibiting altered oxalate metabolism.

Animals↗
PubMed1984

Calcium oxalate retention in subjects with crystalluria.

Calcium oxalate retention was studied in non-stone-forming volunteers. All subjects were placed on a constant diet for 5 days. After the oral administration of 10 microCi of [14C]-oxalic acid, the pattern of urinary oxalate excretion was followed for 48 h. Each subject was then given 10 microCi of [14C]-oxalic acid mixed with sufficient sodium oxalate (7.5 mg/kg body weight) to induce calcium oxalate crystalluria. Urinary oxalate excretion was then recorded for 48 h. After the administration of labeled oxalic acid (without additional sodium oxalate), 76.6 +/- 5.9% of the total recovered dose was excreted by 4 h. When the labeled oxalic acid was mixed with a sodium oxalate load, 62.4 +/- 8.8% was excreted by 4 h (p less than 0.01). Induction of calcium oxalate crystalluria results in the retention of oxalate in the kidney. The degree of retention varies among individuals. Differences in particle retention may help explain the differences between stone formers and non-stone formers.

Adult↗
PubMed1986

The uptake of oxalate by rat liver and kidney mitochondria.

Oxalate, a metabolic end product, forms calcium oxalate deposits in the tissues under a variety of pathological conditions. In order to determine whether oxalate is able to penetrate the mitochondrial matrix, the uptake of oxalate by rat liver and kidney cortical mitochondria was characterized. Mitochondria did not swell in an iso-osmotic medium of ammonium oxalate unless a small amount of phosphate was provided. This phosphate-induced swelling was prevented by N-ethylmaleimide. The uptake of [14C]oxalate by liver and kidney mitochondria followed first order kinetics and was inhibited by mersalyl an inhibitor of the phosphate and dicarboxylate carriers. Accumulation of [14C]oxalate at equilibrium was significantly higher by mitochondria energized with succinate than by rotenone-inhibited mitochondria due to higher matrix pH as determined by the [14C]5,5'-dimethyloxazolidine-2, 4-dione distribution ratio. The velocity of oxalate accumulation by mitochondria was temperature dependent. The activation energy was 81.5 and 86.5 J/mol for liver and kidney mitochondria, respectively. In both types of mitochondria, the rate of oxalate uptake was hyperbolic with respect to the concentration of oxalate. The apparent Km was 28.8 +/- 0.6 and 13.4 +/- 1.2 mM and the Vmax 87.1 +/- 1.1 and 66.1 +/- 3.1 nmol X mg-1 X min-1 at 12 degrees C for liver and kidney mitochondria, respectively. Phenylsuccinate exhibited mixed inhibition of the rate of oxalate uptake. Oxalate exhibited also a mixed inhibition of the uptake and oxidation of malate by mitochondria. The data obtained provide evidence that oxalate is transported across the mitochondrial membrane by a phosphate-linked, carrier-mediated system similar to or identical to the dicarboxylate transporter.

Animals↗
PubMed2003

Angiotensin II involvement in adaptive enteric oxalate excretion in rats with chronic renal failure induced by hyperoxaluria.

UNLABELLED: Enteric secretion of oxalate is induced in rats that have chronic renal failure produced by 5/6 nephrectomy. The purpose of the present study was to examine renal and intestinal handling of oxalate in rats with chronic renal failure (CRF) induced by chronic hyperoxaluria. A rat model for chronic renal failure, induced by chronic hyperoxaluria (CH-CRF), was produced by unilateral nephrectomy combined with dietary ethylene glycol for 4 weeks. Both intact and unilateral nephrectomized rats (UN) without the oxalate load served as controls. Renal handling of oxalate was assessed by measurement of renal clearance of oxalate and creatinine while colonic handling of oxalate and chloride was determined by in vitro transepithelial flux measurements. Angiotensin II mediation was assessed by sensitivity of the transport processes to the AT(1) receptor antagonist losartan. Renal and colonic handling of oxalate in UN rats were similar to intact controls. The CH-CRF rats were hyperoxalemic, hyperoxaluric, and exhibited a twofold increase in oxalate clearance despite a 50% drop in creatinine clearance. Distal (but not proximal) colonic handling of oxalate in CH-CRF rats was reversed from net oxalate absorption seen in UN and intact controls to net secretion that was sensitive to losartan in vitro. CONCLUSION: Although enteric oxalate secretion can be correlated with elevations in plasma oxalate in the absence of overt renal insufficiency by an ANG II-independent mechanism, the present results suggest that some degree of renal insufficiency is necessary to induce ANG II-mediated colonic oxalate secretion.

Adaptation, Physiological↗
PubMed2005

Apoptosis induced by oxalate in human renal tubular epithelial HK-2 cells.

Oxalate is not only considered to be one of the main constituents of urinary stones, but it also has toxic effects on renal tubular epithelial cells, affecting the pathogenesis of nephrolithiasis. We tried to elucidate the effects of oxalate on human renal tubular epithelial cells (HK-2 cells). In addition, we investigated whether the toxic effect of oxalate occurs by apoptosis, and determined the expression of Bcl-2 family and caspase 9 proteins known as apoptosis-related protein. HK-2 cells were incubated with different concentrations of oxalate, and the effect of oxalate on the growth of the cells was assessed by MTT assay. A caspase-3 activity assay and TUNEL assay were performed on HK-2 cells after oxalate exposure in order to evaluate apoptosis. Immunoblot analysis of Bax, Bcl-2, Bcl-xL, and caspase-9 were performed. Oxalate exposure resulted in significant growth inhibition of HK-2 cells as oxalate concentrations increased. The toxic effect of oxalate on HK-2 cells was considered to occur through apoptosis, as suggested by the increase of caspase-3 activity. The percentage of positive nuclei stained using the TUNEL method was 18+/-2.3 in oxalate-treated cells and 2.5+/-0.9 in untreated cells (P<0.05). Bax and caspase-9 protein expression increased significantly as oxalate concentrations increased, but Bcl-2 protein expression decreased. There was no difference in Bcl-xL protein expression among the various concentrations of oxalate. Our results show that oxalate has a toxic effect on HK-2 cells and that this effect is induced by apoptosis, which may be mediated by an intrinsic pathway.

Apoptosis↗
PubMed2006

Chitosan does not reduce post-prandial urinary oxalate excretion.

Chitosan is a positively charged non-absorbable cellulose-like fibrillar biopolymer derived from shellfish which forms films with negatively charged surfaces. We hypothesized that negatively charged oxalate in the intestinal lumen could attach to the positively charged tertiary amino group of chitosan. We studied the effects of chitosan on intestinal oxalate absorption by measuring urinary oxalate excretion following an oral oxalate load with and without accompanying oral chitosan. The subjects consumed a fixed diet and collected urine for 24 h, in divided periods, during control and experimental protocols. Urine was collected with HCl and thymol as a preservative. For the control period, the subjects consumed an oxalate load, 50 g of cooked spinach, with water for lunch; the post-prandial urine collection was divided into three periods of 2 h. For the experimental period, 1 week later, the subjects consumed the same diet as that during the control period, but added 2 g of chitosan to the oxalate load. Post-prandial urinary oxalate excretion was expressed as mg oxalate/g creatinine. The spinach load was associated with a significant post-prandial increase in urinary oxalate during the control period of 25.7+/-12.8 mg/g creatinine. Accompanying the oxalate load with chitosan was well tolerated. There was no decrease in post-prandial urinary oxalate excretion during the experimental period: oxalate excretion rose by 31.3+/-16.9 mg/g creatinine (P=0.57, NS). We conclude that chitosan does not reduce acute intestinal oxalate absorption and therefore does not affect post-prandial urinary oxalate excretion.

Chelating Agents↗
PubMed2004

Oxalate degradation by intestinal lactic acid bacteria in dogs and cats.

This study evaluated the ability of the lactic acid bacteria (LAB) component of canine and feline feces to degrade oxalate in vitro. Oxalate degradation by individual canine-origin LAB was also evaluated. The effects of various prebiotics on in vitro oxalate degradation by selected oxalate-degrading canine LAB was also evaluated. Canine fecal samples reduced oxalate levels by 78 +/- 12.2% (mean +/- S.D.; range: 44-97%, median: 81%). Feline results were similar, with oxalate reduction of 69.7 +/- 16.7% (mean +/- S.D.; range: 40-96%, median: 73%). Thirty-seven lactic acid bacteria were isolated from canine fecal samples. Mean oxalate degradation was 17.7 +/- 16.6% (mean +/- S.D.; range: 0-65%, median: 13%). No oxalate degradation was detected for four (11%) isolates, and 10/37 (27%) degraded less than 10% of oxalate. The effects of lactitol, arabinogalactan, guar gum, gum Arabic, inulin, maltodextrin or a commercial fructooligosaccharide (FOS) product on in vitro oxalate degradation by five canine LAB isolates were highly variable, even within the same bacterial species. Overall, in vitro degradation was significantly greater with guar gum compared to arabinogalactan (P < 0.05), gum Arabic (P < 0.05), and lactitol (P < 0.01). This study suggests that manipulation of the LAB component of the canine and feline gastrointestinal microflora may decrease intestinal oxalate, and correspondingly intestinal oxalate absorption and renal excretion, thus potentially reducing oxalate urolithiasis.

Animals↗
PubMed1984

Oxalate removal by hemodialysis in end-stage renal disease.

Because of mounting evidence of precipitation of calcium oxalate in the soft tissues of patients with end-stage renal disease (ESRD) on maintenance hemodialysis, the plasma oxalate concentrations and calculated dialysis removal of oxalate were studied in seven patients without evidence of either primary or absorption hyperoxaluria prior to ESRD. A reversed-phase high-pressure liquid chromatographic method was developed to quantitate serum oxalate. Mean value +/- SE in four healthy controls was 28 +/- 5 mumol/L, and in the seven patients it was 187 +/- 15 mumol/L predialysis and 89 +/- 11 mumol/L postdialysis. Oxalate deposition in the soft tissues of ESRD patients is the consequence of sustained hyperoxalemia. Oxalate removal by dialysis was calculated from the four-hour oxalate clearance. Since the ionic radii of phosphate and oxalate are similar, total oxalate clearance was calculated midpoint of dialysis. Mean oxalate removal/dialysis was 3.01 +/- 0.283 mmol. On a daily basis this value was 1.645 +/- 0.155 mmol, which is about threefold the normal oxalate excretion rate. It is not significantly different from the excretion rate in absorption oxalurias but is less than that in primary hyperoxaluria. Therefore, it is concluded that hyperoxalemia in ESRD results from loss of renal excretion, failure of hemodialysis to remove enough oxalate to maintain a normal serum concentration, and increased intestinal absorption of oxalate and/or increased endogenous production.

Adult↗
PubMed1980

The production of (14C) oxalate during the metabolism of (14C) carbohydrates in isolated rat hepatocytes.

Oxalate (14C) was produced during the metabolism of (U-14C) carbohydrates in hepatocytes isolated from normal rats. At 10 mM, the order of oxalate production was fructose > glycerol > xylitol > sorbitol greater than or equal to glucose in the ratio 10 : 4 : 3 : 1 : 1. This difference between oxalate production from fructose and glucose was reflected in their rates of utilisation, glucose being poorly metabolised in hepatocytes from fasted rats. Fructose was rapidly metabolised, producing glucose, lactate and pyruvate as the major metabolites. Glycerol, xylitol and sorbitol were metabolised at half the rate of fructose, the major metabolites being glucose, lactate and glycerophosphate. The marked similarity in the pattern of intermediary metabolites produced by these polyols was not, however, reflected in the rates of oxalate production. Hepatic polyol metabolism resulted in high levels of cytosolic NADH, as indicated by elevated lactate : pyruvate and glycerophosphate : dihydroxyacetone phosphate ratios. The artificial electron acceptor, phenazine methosulphate (PMS) stimulated oxalate production from the polyols, particularly xylitol. In the presence of PMS, the order of oxalate production was fructose greater than or equal to xylitol > glycerol > sorbitol in the ratio 10 : 10 : 6 : 2. The production of glucose, lactate and pyruvate from the polyols was also stimulated by PMS, whereas the general metabolism of fructose, including oxalate production, was little affected. Oxalate (14C) was produced from (1-14C), (2-14C) and (6-14C) but not (3,4-14C) glucose in hepatocytes isolated from non-fasted, pyridoxine-deficient rats. Whilst this labelling pattern is consistent with oxalate being produced by a number of pathways, it is suggested that metabolism via hydroxypyruvate is a major route for oxalate production from various carbohydrates, with perhaps the exception of xylitol, which appears to have an alternative mechanism for oxalate production. The observation that carbohydrates, particularly fructose, contribute to endogenous oxalate production lends support to the hypothesis that a high sucrose consumption contributes to the formation of renal oxalate stones in man.

Animals↗
PubMed1996

Urinary oxalate excretion increases with body size and decreases with increasing dietary calcium intake among healthy adults.

Increasing dietary calcium intake decreases urinary oxalate excretion by increasing intestinal precipitation of dietary oxalate as calcium oxalate. This mechanism was speculated to account for the decreased prospective incidence of kidney stones as estimated dietary calcium intake, adjusted for caloric intake, increased among men in a recent large epidemiological study. To further assess the relationship between estimated diet calcium and urinary oxalate, we studied 94 health adults, 50 women and 44 men, ages 20 to 70 years with weights ranging form 47 to 104 kg while they ate their customary diets. Each subject completed a semiquantitative food frequency questionnaire and collected three 24-hour urines preserved with HCl. The urines were collected accurately as judged by a mean intrasubject CV for creatinine excretion of 9.8% and direct relations between urinary creatinine excretion and body wt (r = 0.62; P < 0.0001), or predicted urine creatinine content for sex, age and weight using the Cockcroft and Gault formulas (r = 0.76; P < 0.0001). Estimated diet calcium intake ranged from 6.8 to 68 mmol/day (272 to 2720 mg/day) and averaged 29.5 mmol/day (1180 mg/day). Individual mean urinary oxalate excretion ranged from 0.079 go 0.332 mmol/day (7 to 29 mg/day) and averaged 0.198 mmol/day (17 mg/day). Among all subjects, daily oxalate excretion was directly related to creatinine excretion as an estimate of lean body mass (r = 0.61; P < 0.0001). Thus, oxalate excretion among men averaged 0.228 +/- 0.051 SD mmol/day, a value significantly higher than the average among women of 0.173 +/- 0.045 mmol/day (P < 0.001). Daily urine oxalate excretion/creatinine decreased curvilinearly as estimated dietary Ca intake increased (r = -0.30; P = 0.0035) and as the ratio of estimated dietary calcium to dietary oxalate increased (r = -0.39; P = 0.0001). We conclude that body size is the major determinant of urinary oxalate excretion among healthy adults, presumably reflecting variations in endogenous oxalate synthesis with lean body mass. Increasing estimated diet calcium intake, especially up to the range of 15 to 20 mmol/day (600 to 800 mg/day) has an additional effect to decrease during oxalate excretion, presumably by limiting intestinal absorption of dietary oxalate.

Adult↗
PubMed1981

Urine composition in normal subjects after oral ingestion of oxalate-rich foods.

1. Urinary composition was studied in nine healthy adults on unrestricted diet and low-oxalate diet with and without individual oxalate-rich foods. 2. Urine oxalate was constant on the low-oxalate and constant high-oxalate diets and only fluctuated greatly on unrestricted diet. 3. Urine oxalate was mainly due to dietary oxalate which accounts for up to two-thirds of urinary oxalate. 4. Urine oxalate was unaffected by urine volume. 5. Varying percentages of dietary oxalate were absorbed depending on the nature of the foodstuff. 6. Although tea was the main source of dietary oxalate in some people it, like strawberries, did not represent a real risk factor. Chocolates, peanuts, beetroot, rhubarb and spinach were considered as high-risk foods. 7. Calcium oxalate crystalluria at 4 degrees C was increased significantly when the oxalate-rich foods were taken. When urine was examined at 37 degrees C no increase in crystalluria was found.

Adult↗
PubMed1979

Oxalate loading test: a screening test for steatorrhoea.

To investigate the possibility of measuring urinary oxalate output instead of faecal fat excretion as an outpatient screening test for steatorrhoea, we determined 24 hour urinary oxalate and five day faecal fat excretion before and during an oral load of sodium oxalate 600 mg daily (oxalate 4.44 mmol), in 32 patients with suspected malabsorption on a diet containing oxalate 30 mg (0.33 mmol), fat 50 g (180 mmol), and calcium 1 g (25 mmol). Nineteen patients proved to have steatorrhoea (mean faecal fat 62 mmol/24 h, range 19--186 mmol) of varying aetiologies. On the diet alone, urinary oxalate was raised in only nine of these patients (mean 0.25 mmol/24 h, range 0.08--0.59 mmol) (normal less than 0.20). By contrast, when the diet was supplemented with oral sodium oxalate, all 19 patients with steatorrhoea had hyperoxaluria (mean 0.91 mmol/24 h, range 0.46--1.44 mmol) (normal less than 0.44). There was a significant positive linear relationship between urinary oxalate and faecal fat when the 32 patients were on the high oxalate intake (r = 0.73, P less than 0.001), but not when they were on the low oxalate intake. Mean percentage absorption of orally administered oxalate was 5.8 +/- 0.99% (+/- 1 SD) in normal subjects and 14.7 +/- 6.0% (P less than 0.002) in patients with steatorrhoea. Measurement of urinary oxalate output during oral sodium oxalate loading appears to be a reliable and convenient screening test for steatorrhoea.

Adult↗
PubMed2001

Ultrastructure of selected calcium oxalate-containing urinary calculi from dogs.

OBJECTIVE: To elucidate the ultrastructural details of calcium oxalate-containing urinary calculi from dogs. Sample Population-38 specimens selected from a collection of 8,297 oxalate-containing urinary calculi from dogs: 22 specimens composed of calcium oxalate (calcium oxalate monohydrate [COM], calcium oxalate dihydrate [COD], or COM and COD) and 16 specimens composed of calcium oxalate with amorphous calcium phosphate. PROCEDURE: Analyses of specimens included use of plain, reflected, and polarized light microscopy, X-ray diffractometry, scanning electron microscopy (SEM) with backscattered electron (BSE) imagery, and electron microprobe analysis. RESULTS: Four texture types were observed in calcium oxalate calculi; 4 texture types of calcium oxalate-calcium phosphate-mixed calculi were recognized. Texture types were delineated through differences in calcium oxalate crystal sizes, which were affected by urine supersaturation and abundance of crystal nucleation sites. Segregation of calcium oxalate from calcium phosphate indicated they do not precipitate under the same conditions. Deposition of calcium phosphate between calcium oxalate crystals decreased the volume of pore spaces within calculi. Porosity was observed along boundaries between COM and COD. Minute pores increased the surface area of calculi exposed to urine, and this increase in liquid-solid interface promotes interaction of crystals with the surrounding urine. CONCLUSIONS AND CLINICAL RELEVANCE: Calcium oxalate urolithiasis is of major concern, because it is often a recurrent disease among dogs, principally treated by surgical removal of calculi, with few effective dissolution strategies. Understanding the ultrastructure and mineralogic content of calcium oxalate and its association with amorphous calcium phosphate is a step toward the solution of this increasingly important medical problem.

Animals↗
PubMed1991

[Studies of sodium pentosan polysulphate (SPP) therapy on the urinary stone disease. Experimental studies on the calcium oxalate crystallization and the effects in healthy subjects].

Concerning with the inhibitory activity of sodium pentosan polysulphate (SPP) on calcium oxalate stone formation, the following three experiments were carried out. 1) The inhibitory activities for calcium oxalate crystal formation, aggregation and growth in vitro, 2) the effects on the deposition of calcium oxalate crystals in rats treated with ethylene glycol, and 3) the effects of oral administration to human subjects on the metastable limit of urinary calcium oxalate and on the inhibitory activity of the urine for calcium oxalate crystal growth. The results were as follows: 1. The degree of the calcium oxalate crystal formation measured by an aggregometer was decreased by addition of more than 1 mM of SPP. 2. The inhibitory activity of SPP on calcium oxalate crystal aggregation was measured using a Coulter Counter. The aggregation was inhibited at a low concentration of SPP (0.02 microM). 3. Calcium oxalate crystal growth was measured using a seeded crystal method with [14C] oxalic acid. SPP inhibited the crystal growth proportionally to the concentration of SPP (0.1 microM-100 microM). 4. Renal tubular deposition of calcium oxalate crystals was marked in rats that orally received ethylene glycol (0.4%), which was expected to be suppressed by intramuscular administration of SPP (30 mg/kg/day or 60 mg/kg/day). 5. Oral administration of SPP (500 mg/day) to five healthy male subjects for five days resulted a tendency to increase of the metastable limit of the urinary calcium oxalate as measurement by an aggregometer, but the inhibitory activity of the urine for calcium oxalate crystal growth, which was measured by seeded crystal method with [14C] oxalic acid, showed no variable changes.

Adult↗
PubMed1999

Oxalate: from crystal formation to crystal retention.

Idiopathic calcium oxalate stone formation is a multifactorial disease. It is therefore unlikely that a single underlying condition will be responsible for entire spectrum of the disease; however, it appears that one important factor in the pathogenesis is an abnormality in oxalate metabolism. Whatever the cause, two critical parameters for stone formation are crystal formation and crystal retention in the renal tubules. Although crystal formination and role of oxalate in crystal formation have been evaluated extensively, it is only recently that crystal retention has been addressed. Previous studies from our laboratories demonstrated that oxalate exposure to renal epithelial cells in culture resulted in initiation of a program of events including DNA synthesis and cell death. The present studies evaluated effects of oxalate on cell proliferation and damage to distal tubular (Madin-Darby canine kidney cells) and proximal (LLC-PK1 cells) cells. Effects of oxalate exposure on calcium oxalate monohydrate (COM) crystal adherence to these cells were also evaluated. Results presented herein demonstrate that proximal tubular cells are more sensitive to oxalate than distal tubular cells. Furthermore, oxalate exposure to proximal tubular cells resulted in reinitiation of DNA synthesis, whereas no such effect was observed in distal tubular cells. Higher levels of oxalate (> 1 mM) resulted in cell loss of both proximal and distal tubular cells, as observed by crystal violet staining. Despite these differences, oxalate exposure to both proximal and distal tubular cells resulted in increased COM crystal adherence. Thus, oxalate exposure may promote crystal adherence to renal epithelial cells either secondarily to cell death and proliferation or by a yet unidentified mechanism. These studies provide the first direct evidence for the role of oxalate in promoting COM crystal retention by the urothelium.

Animals↗
PubMed2002

Neurotoxic effects of carambola in rats: the role of oxalate.

BACKGROUND AND PURPOSE: Carambola (star fruit) has been reported to contain neurotoxins that cause convulsions, hiccups, or death in uremic patients, and prolong barbiturate-induced sleeping time in rats. The constituent responsible for these effects remains uncertain. Carambola contains a large quantity of oxalate, which can induce depression of cerebral function and seizures. This study was conducted to investigate the role of oxalate in carambola toxicity in rats. MATERIALS AND METHODS: The effects on barbiturate-induced sleeping time and death caused by intraperitoneal administration of carambola juice were observed in Sprague-Dawley rats. To obtain a dose-dependent response curve and evaluate the lethal dose, rats were treated with serial amounts of pure carambola juice diluted with normal saline in a volume of 1:1. To test the role of oxalate in the neurotoxic effect of carambola, either 5.33 g/kg carambola after oxalate removal or 5.33 g/kg of pure carambola juice diluted with normal saline were administered intraperitoneally, while the control group was given normal saline before pentobarbital injection. The effects of carambola and oxalate-removed carambola on barbiturate-induced sleeping time were compared with those of saline. To assess the lethal effect of oxalate in carambola, we gave rats chemical oxalate at comparable concentrations to the oxalate content of carambola. RESULTS: Carambola juice administration prolonged barbiturate-induced sleeping time in a dose-dependent manner. The sleeping time of rats that received normal saline and 1.33 g/kg, 2.67 g/kg, 5.33 g/kg, and 10.67 g/kg of carambola juice were 66 +/- 16.6, 93.7 +/- 13.4, 113.3 +/- 11.4, 117.5 +/- 29.0, and 172.5 +/- 38.8 minutes, respectively. The three higher-dose groups had longer sleeping times than controls (p < 0.05 or 0.005). This effect was eliminated after the removal of oxalate from carambola juice. Four of eight rats in the 10.67-g/kg group and all rats in the 21.33 g/kg and chemical oxalate groups died after seizure. Lethal doses of carambola juice were rendered harmless by the oxalate removal procedure. CONCLUSIONS: Oxalate is a main constituent of carambola neurotoxicity. This finding suggests that patients with carambola intoxication should be treated for oxalate toxicosis.

Animals↗
PubMed1996

Characterization of nuclear oxalate binding protein of rat and human kidney.

PURPOSE: To characterize the nuclear oxalate binding protein and its involvement in hyperoxaluria. MATERIALS AND METHODS: Rat and human renal cortical epithelial cell nuclear protein was isolated and studied. Renal nuclear histones were isolated by acid extraction and purified by ion exchange column chromatography. RESULTS: Most of the 14C-oxalate binding was present in the histone-H1 fraction. The oxalate binding activity resided exclusively in the H1B fraction of H1. The protein was purified 13 to 16-fold with a specific activity of 940 to 1570 pmol./mg. protein. Oxalate binding to rat or human kidney or calf thymus histone was rapid, reversible, pH dependent and saturable. Trypsin treatment abolished the binding activity. Scatchard plot analysis revealed the presence of 2 distinct oxalate binding sites, one with high affinity and the other with low affinity. Oxalate binding was inhibited by DIDS (4,4'-diisothio-cyanostilbene-2, 2'-disulfonic acid) and other dicarboxylate transport inhibitors. The IC50 values for different substrate analogues were, in decreasing order, oxalate < oxamate < succinate < glyoxylate < malate < glycolate. In experimental urolithic rats, histone oxalate binding was increased by 50 to 70%. The higher oxalate binding activity in hyperoxaluric rats was due to increased formation of H1. Histone exhibited in vitro calcium oxalate crystal growth promoter activity. CONCLUSION: Oxalate binding activity resided in the H1B of histone H1. The protein promoted calcium oxalate crystal growth. This suggested a possible role for this protein in the retention of calcium oxalate in the nucleus.

Animals↗