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PubMed1990

Sulfate and oxalate exchange for bicarbonate across the basolateral membrane of rabbit ileum.

The purpose of these studies was to further define the transport of SO4(2-) and oxalate across the basolateral membrane (BLM) of rabbit ileum. We previously found evidence for Cl-(-)SO4(2-) exchange but no evidence for carrier-mediated oxalate transport. A HCO3- gradient (but not a pH gradient) was found to stimulate SO4(2-) and oxalate uptake in BLM vesicles; uptake was inhibited by DIDS. Oxalate cis-inhibited HCO3- gradient SO4(2-) uptake and trans-stimulated SO4(2-) uptake, suggesting SO4(2-) and oxalate used the same carrier (SO4(2-)- and oxalate-HCO3-exchange). Cl- had no effect on HCO3- gradient-stimulated SO4(2-) uptake, indicating that Cl(-)-SO4(2-) exchange was a different carrier. Other substrates found to be transported on the HCO3- exchanger were oxaloacetate and S2O3(2-)-.SO4(2-), S2O3(2-). and oxalate were found to also use the SO4(2-)-Cl- exchanger, whereas oxalate was only transported on the HCO3- exchanger. SO4(2-)-HCO3- exchange was found on villus, but not crypt cell, BLM. These results indicate that there is a SO4(2-)-HCO3- exchanger on the BLM of villus cells that also transports oxalate, and along with our previous studies, the results provide evidence for the transepithelial transport of oxalate.

Animals↗
PubMedDate not supplied

Oxalate-induced redistribution of phosphatidylserine in renal epithelial cells: implications for kidney stone disease.

AIMS: The present studies assessed the possibility that exposure to oxalate leads to alterations in membrane structure that promote crystal binding to renal epithelial cells. Specifically, we determined whether oxalate exposure produces a redistribution of membrane phosphatidylserine (PS) and an increase in the binding of (14)C-oxalate crystals to renal epithelial cells. METHODS: PS distribution was monitored in MDCK cells and in phospholipid-containing vesicles using NBD-PS, a fluorescent derivative of PS. Superficial PS was also detected by monitoring the binding of annexin V to MDCK cells. RESULTS: Oxalate exposure rapidly increased the abundance of superficial NBD-PS and increased the binding of annexin V to MDCK cells. Oxalate exposure also increased PS at the surface of phospholipid vesicles, suggesting that oxalate may interact directly with PS. The oxalate concentrations that increased superficial PS also increased binding of (14)C-oxalate crystals to MDCK cells, and the increased crystal binding was blocked by annexin V. CONCLUSIONS: These findings provide direct evidence that oxalate exposure promotes both a redistribution of PS and an increase in crystal binding in renal epithelial cells and support the notion that oxalate toxicity may contribute to the development of stone disease by altering the properties of the renal epithelial cell membrane.

Animals↗
PubMed2005

Importance of magnesium in absorption and excretion of oxalate.

INTRODUCTION: Magnesium treatment for calcium oxalate urolithiasis is discussed controversially. The aim of this study was to investigate the influence of magnesium supplementation on the oxalate absorption. MATERIALS AND METHODS: The [13C2]oxalate absorption test was always performed three times in 6 healthy volunteers under standardized conditions, with one 10-mmol magnesium supplement together with the labeled oxalate and with two 10-mmol magnesium supplements given in 12-hour intervals. RESULTS: The mean intestinal oxalate absorption under standard conditions was 8.6 +/- 2.83%. The oxalate absorption with one 10-mmol magnesium supplement was 5.2 +/- 1.40% and with two supplements 5.5 +/- 1.62%. Both decreases were statistically significant relative to the standard test, however, not significantly different from each other. CONCLUSIONS: The results show that magnesium administration decreases the oxalate absorption, when magnesium is taken together with oxalate. However, magnesium administration does not decrease the oxalate absorption, when magnesium and oxalate intake differ by 12 h.

Absorption↗
PubMed1994

Intestinal excretion of oxalate in chronic renal failure.

The extrarenal elimination of oxalate via the intestine was studied in rats with chronic renal failure by measuring the magnitude and direction of oxalate fluxes across the small and large intestine. Oxalate transport was determined in vitro across short-circuited sheets of jejunum, ileum, and colon that were placed in Ussing chambers. The concentration of oxalate in plasma and urine was measured immediately before the transport studies. The results show that, 6 wk after 5/6 nephrectomy, rats with chronic renal failure have lower (decreases 50%) renal clearance of oxalate and a higher mean plasma oxalate concentration (increases 80%) than controls. The basal absorption of oxalate across the colon was changed to secretion in animals with chronic renal failure (from 12.81 +/- 2.22 (N = 9) to -14.96 +/- 2.57 (N = 11) pmol/cm2 per hour). Both the jejunum and the ileum supported a basal net secretory flux of oxalate (-19.71 +/- 2.39 (N = 13) and -30.06 +/- 2.80 (N = 16) pmol/cm2 per hour) that was unaffected by renal insufficiency. These studies demonstrate that intestinal transport systems for oxalate are altered in experimental chronic renal failure, and the distal colon is identified as the primary site for this adaptive response. In chronic renal failure, the entire intestinal tract can potentially excrete oxalate.

Animals↗
PubMed1978

Urinary oxalate excretion related to ileocolic surgery in patients with Crohn's disease.

Urinary oxalate excretion was studied in healthy subjects and before and after surgery in patients with Crohn's disease. Urinary oxalate excretion in relation to the length of diseased or resected ileal segment in patients subjected to restorative and colectomy procedures, as well as in relation to faecal excretion of fat and bile salts and to urinary excretion of vitamin B12 and calcium, was also studied. The studies were performed in patients on a free diet or standard hospital diet and on a high-oxalate and/or high-fat diet. When patients subjected to ileal resection in conjunction with minor colonic resection were studied on a high-oxalate diet, urinary oxalate excretion increased with length of ileum resected and correlated with faecal fat excretion and urinary excretion of vitamin B12 but not with faecal excretion of bile salts. Increasing the dietary fat intake in these patients further increased urinary oxalate excretion. Although urinary oxalate excretion increased somewhat in colectomized patients on a high-oxalate diet, indicating an increased absorption of dietary oxalate, this increase showed no correlation either to faecal fat or bile salt excretion, or to urinary excretion of vitamin B12. The result are consistent with the "solubility theory". A diet low in fat and oxalate and high in calcium is recommended in patients with hyperoxaluria.

Adult↗
PubMed2000

Urinary oxalate, glycolate, glyoxylate, and citrate after acute intravenous administration of glyoxylate in rats.

BACKGROUND AND PURPOSE: Urinary oxalate plays an important role in the formation of calcium oxalate renal stones, and approximately 50% to 60% of urinary oxalate is derived from the endogenous metabolism of glyoxylate. Therefore, we measured urinary oxalate, glycolate, glyoxylate, and citrate concentrations after acute intravenous administration of various doses of glyoxylate in rats to study oxalate metabolism. MATERIALS AND METHODS: Male Wistar rats weighing approximately 200 g were divided into six groups of eight animals each. Anesthetized rats received glyoxylate (0, 1, 2, 5, 10, and 20 mg) intravenously. Urine specimens were collected before and every hour after each dose for 4 hours, and the concentrations of oxalate, glycolate, glyoxylate, and citrate were measured by capillary electrophoresis. RESULTS: Hourly oxalate excretion in the urine peaked at 1 hour after glyoxylate administration, and the peak concentration increased in a dose-dependent manner. Approximately 15% to 30% (mol/mol) of the dose was converted to oxalate within 4 hours and 2% to 4.6% was converted to glycolate. Urinary glyoxylate was not detectable before glyoxylate administration, but large doses resulted in a significant amount of glyoxylate (0.7%-2.3%) appearing in the urine, and the level peaked at 1 hour after administration. Urinary glycolate also peaked at 1 hour after administration of glyoxylate. The urinary citrate concentration generally decreased by 3% to 33% after each dose of glyoxylate, except that it increased slightly after the 20-mg dose. CONCLUSION: Administration of glyoxylate increased urinary oxalate and glycolate excretion in rats, supporting the importance of the glycolate-glyoxylate-oxalate pathway.

Animals↗
PubMed2006

[Effect of oral lactosucrose supplementation on human enteric oxalate-degrading bacteria].

A variety of oxalate-degrading bacteria including Oxalobacter formigenes and some species of Bifidobacterium are known to colonize the human intestinal tract. Oral lactosucrose supplementation promotes the growth of Bifidobacterium in the human intestine. Therefore, we investigated the effect of oral lactosucrose supplementation on enteric oxalate-degrading bacteria in twelve healthy men (age ranging from 25 to 39 years). Lactosucrose was orally administered 10 g daily for 2 weeks without restriction of dietary intake. The total number of oxalate-degrading bacteria in feces and the 24-hour urinary excretion of oxalate were examined before and after lactosucrose supplementation. The total number of oxalate degrading-bacteria was significantly increased by lactosucrose supplementation (9.20 +/- 0.44 versus 9.77 +/- 0.46, p<0.05), although there was no significant change in the urinary oxalate excretion. The oxalate degrading-bacteria isolated from feces was biochemically identified as Bifidobacterium adolescentis. In conclusion, oral supplementation of 10 g lactosucrose daily for 2 weeks was effective in multiplying oxalate-degrading bacteria, but not in reducing urinary oxalate excretion under free non-restricted dietary intake. In addition, it was suggested that various species of Bifidobacterium were related to degradation of oxalate in the human intestine.

Administration, Oral↗
PubMed1991

Prevalence of calcium oxalate uroliths in miniature schnauzers.

Epidemiologic data were evaluated from all dogs admitted to the University of Minnesota, Veterinary Teaching Hospital (UMVTH) between June 1981 and November 1989. Of 69,890 admissions, 2,077 were Miniature Schnauzers. Uroliths were retrieved from 63 of the 2,077 Miniature Schnauzers admitted. In 20 of the 63 urolith episodes, calcium oxalate was the predominant mineral identified. By comparison, calcium oxalate uroliths were identified in only 56 of the remaining 67,813 non-Miniature Schnauzer canine admissions. The odds that uroliths from Miniature Schnauzers were composed of calcium oxalate was 11.8 times greater than for other canine breeds evaluated at the UMVTH (95% confidence interval = 6.8 to 20.1). Data also were evaluated from files of uroliths retrieved from dogs and submitted to the Minnesota Urolith Center for quantitative mineral analysis, between June 1981 and November 1989. Of 3,930 uroliths analyzed, 615 (15.6%) uroliths were obtained from Miniature Schnauzers. of the 615 uroliths, 175 (28.4%) were calcium oxalate. By comparison, only 550 (16.6%) of the remaining 3,315 from dogs of breeds other than Miniature Schnauzers were calcium oxalate. The odds that uroliths submitted for analysis were composed of calcium oxalate was 2 times greater for Miniature Schnauzers than for dogs of other breeds (95% confidence interval = 1.6 to 2.4). Calcium oxalate uroliths were retrieved more frequently in males than females. The risk for males developing calcium oxalate uroliths was greater than 3 times the risk for females in both groups of data evaluated. The mean age of all Miniature Schnauzers admitted to the UMVTH with calcium oxalate uroliths was 9 years. Calcium oxalate uroliths were not detected in Miniature Schnauzers younger than 1.7 years.

Age Factors↗
PubMed1979

Gas-chromatographic estimation of urinary oxalate and its comparison with a colorimetric method.

We describe a simple, specific gas-chromatographic method for urinary oxalate. Its specificity was evaluated by precipitating the oxalate as its calcium salt from urine, followed by methylation of the oxalate with boron trifluoride/methanol and subsequent gas-chromatographic separation and quantitation of the dimethyl oxalate. [U-14C]Oxalate and n-decanoic acid are used as internal standards. Analytical recoveries ranged from 93.8 to 97.7% for oxalate-supplemented urine. Twenty replicate analyses of urines containing typical concentrations of oxalate gave CVs of 10.0, 9.1, and 8.3% for low, medium, and high concentrations, respectively. Day-to-day precision (CV) for single analyses repeated on 20 days was 8.6% for the low urinary oxalate concentration. The lower limit of detection of urinary oxalate is 25 mumol/L. Results by our method correlated well (r = 0.95) with those by a colorimetric method (Clin. Chim. Acta 36: 127, 1972) but averaged 68.4% of those obtained colorimetrically (n = 75 samples, p less than 0.001). The expected range for our method is calculated to be 80 to 500 mumol of oxalate per 24-h urine (mean +/- 1 SD: 280 +/- 100).

Adult↗
PubMed1983

[Clinical aspects of oxalate metabolism].

The daily amount of oxalate in normales is formed by about 90 per cent from endogenous sources. Approximately 10 per cent are due to intestinal absorption of dietary oxalate. The oxalate formed endogenously is derived from aminoacid-, carbohydrate- and ascorbic acid metabolism. Oxalate synthesis is increased in inherited defects of enzymes (primary hyperoxaluria) or as a consequence of exogenous factors (vitamin-B6-deficiency, ethylene glycol intoxication, high dose ascorbic acid application, possibly excessive protein and carbohydrate intake). The intestinal absorption of oxalate is increased in some diseases of the intestinal tract (Morbus Crohn, ulcerative colitis). Oxalate, that is totally excreted in urine, is the principal component for urinary calcium oxalate saturation. Oxalate accumulates in renal failure. The increased plasma oxalate level - as a consequence of impaired renal function and additional metabolic influences - is an important factor for calcium oxalate depositions in uremic patients.

Animals↗
PubMed1999

Effect of sex hormones on oxalate-synthesizing enzymes in male and female rat livers.

PURPOSE: We studied the effect of changes in sex hormones on oxalate metabolism in rats. MATERIALS AND METHODS: Adult male and female rats were administered a precursor of oxalate, and the relationship between dose and urinary oxalate was examined. Levels of sex hormones were varied in rats and glycolate oxidase (GO) and serine pyruvate aminotransferase (SPT) activities were measured under the conditions of being fed tap water or loading with 0.5% ethylene glycol. In addition, urinary oxalate excretion was evaluated. RESULTS: Ethylene glycol and glycolate increased urinary oxalate concentration in male rats dose-dependently but less in female rats. There was almost no change during glycine loading in either male or female rats. GO activity was significantly lower in intact female and gonadectomized male rats. SPT activity was slightly higher in the female than in the male controls. There were no differences in urinary oxalate excretions between male and female rats. During ethylene glycol loading, GO and SPT activities were similar to those with tap water intake. However, urinary oxalate excretion increased to two times the control value in male rats but only slightly increased in female rats. CONCLUSIONS: Sex-related differences exist in the metabolic conversion of glycolate to oxalate in rats, and GO activity is promoted by testosterone. Although difference in GO activity has no physiological effect on oxalate synthesis, GO activity affects urinary oxalate excretion during ethylene glycol loading. We could also conclude that estrogen decreases GO activity in male rats from our results.

Alcohol Oxidoreductases↗
PubMed1982

Oxalate transfer across the membranes of sarcoplasmic reticulum during the uptake of Ca++.

The kinetic profile of Ca++ uptake in the presence of oxalate is biphasic. An initial phase independent on oxalate is followed by an oxalate-dependent phase delayed in time. The ionophore X-537A only abolishes the net Ca++ uptake if added before the onset of the oxalate phase. However, during this phase, X-537A suddenly releases an amount of Ca++ similar in quantity to that released in the initial phase. The delay of the oxalate-dependent phase is a function of pH. At pH of about 5.5, the oxalate phase and simultaneous calcium oxalate precipitation would theoretically start at the beginning, with no delay. Ejection of protons during Ca++ uptake is strongly depressed by oxalate, but not by other organic anions which do not trap Ca++. It is suggested that oxalate is transferred to the inside of the vesicles as a monoprotonated species at expense of protons ejected by the Ca++-pump during the uptake of Ca++.

Animals↗
PubMed1984

Postprandial hyperoxaluria and intestinal oxalate absorption in idiopathic renal stone disease.

Calcium and oxalate were studied in daily, fasting and postprandial urine specimens from healthy subjects and patients with idiopathic renal calcium stones in response to a test meal free of oxalate, and supplemented with calcium and 14carbon-oxalic acid. The data showed that the amount of oxalate in fasting urine of patients with stones did not differ from that in controls. Generally, patients with stones had considerable postprandial hyperoxaluria in terms of excretion and concentration, associated with a significantly higher degree of supersaturation with regard to calcium oxalate compared to controls. These findings were paralleled by decreased intestinal absorption of 14carbon-oxalate and by unchanged 24-hour urinary oxalate. Although the source of increased postprandial oxalate in patients with stones is not clear the possibility of enhanced de novo synthesis from oxalate precursors is discussed. In patients with different types of calciuria the 2 main risk factors (hyperoxaluria and hypercalciuria) for the process of stone formation are recognizable more readily in the postprandial urine specimens than in fasting or daily urine specimens.

Adult↗
PubMed2004

The impact of dietary oxalate on kidney stone formation.

The role of dietary oxalate in calcium oxalate kidney stone formation remains unclear. However, due to the risk for stone disease that is associated with a low calcium intake, dietary oxalate is believed to be an important contributing factor. In this review, we have examined the available evidence related to the ingestion of dietary oxalate, its intestinal absorption, and its handling by the kidney. The only difference identified to date between normal individuals and those who form stones is in the intestinal absorption of oxalate. Differences in dietary oxalate intake and in renal oxalate excretion are two other parameters that are likely to receive close scrutiny in the near future, because the research tools required for these investigations are now available. Such research, together with more extensive examinations of intestinal oxalate absorption, should help clarify the role of dietary oxalate in stone formation.

Animals↗
PubMed1998

Genetic and dietary influences on urinary oxalate excretion.

Several genes contribute to the development of calcium oxalate nephrolithiasis as it is a polygenic disease. To explore the influence of genetic factors on oxalate excretion we have examined the distribution of oxalate excretions in 101 normal individuals who consumed self-selected diets. The distribution was apparently trimodal, consistent with the existence of three classes of oxalate excretors reflecting two allelic genes determining high and low oxalate excretion occurring with frequencies of 0.32 and 0.68 respectively. The pattern of inheritance in eight families was compatible with the expression of a pair of codominant alleles. A comparison of the distribution of excretory classes among the 101 normal individuals with that of 101 calcium oxalate stone formers suggests that high oxalate excretion may be associated with a 4-fold increased risk of stone disease and intermediate excretion with a 1.6-fold increase. Control of dietary factors influencing oxalate excretion apparently improved the discrimination between excretory classes in 17 individuals but the intra-individual variability in oxalate excretion was not reduced in four of nine individuals in whom this parameter was evaluated. More stringent dietary control than that applied in this study may be required before more extensive genotyping of individuals is attempted.

Adult↗
PubMed1992

Acute hyperoxaluria, renal injury and calcium oxalate urolithiasis.

Single intraperitoneal injections of three, seven, or 10 mg. of sodium oxalate per 100 gm. of rat body weight were administered to male Sprague-Dawley rats. At various times after the injection, urine samples were analyzed for oxalate, and urinary enzymes, alkaline phosphatase, leucine aminopeptidase, gamma-glutamyl transpeptidase, and N-acetyl-beta-glucosaminidase. The kidneys were processed for light microscopy and renal calcium and oxalate determination. Oxalate administration resulted in an increase in urinary oxalate and formation of calcium oxalate crystals in the kidneys. The amount and duration of urinary excretion of excess oxalate and retention of crystals in the kidneys correlated with the dose of sodium oxalate administered. At a low oxalate dose of three mg./100 gm., crystals moved rapidly down the nephron and cleared the kidneys. At higher doses crystals were retained in kidneys and at a dose of 10 mg./100 gm. were still there seven days post-injection. Crystal retention was associated with enhanced excretion of urinary enzymes indicating renal tubular epithelial injury.

Acute Disease↗
PubMed1991

Plasma oxalate in patients with chronic renal failure receiving continuous ambulatory peritoneal dialysis or hemodialysis.

Plasma oxalate was measured in 20 patients receiving continuous ambulatory peritoneal dialysis (CAPD) and 20 patients receiving hemodialysis (HD). All patients had levels well above the reference range of less than 2.0 to 5.0 mumol/L (less than 0.18 to 0.44 mg/L), the medians being 34 mumol/L (2.99 mg/L) and 42 mumol/L (3.70 mg/L) for the two groups, respectively. Plasma oxalate did not differ significantly in the two groups. Plasma oxalate was not influenced by the number of months patients had received dialysis treatment, but a significant correlation was found between oxalate and creatinine in the 40 patients studied (P less than 0.02, r = 0.38). Predialysis oxalate levels were reduced by approximately 60% following HD, but returned to 80% of the predialysis levels within 24 hours and 95% within 48 hours. Oxalate levels did not differ significantly in samples taken before, during, and after exchanges of CAPD fluid. That the patients treated with CAPD did not have higher oxalate levels than the HD group suggests that the continuous nature of the former treatment compensates for the lower oxalate clearance by the peritoneum. The reported higher risk of oxalosis associated with intermittent peritoneal dialysis has led to a similar risk being postulated for CAPD; however, the present study indicates that if such a risk exists, it cannot be explained by higher levels of oxalate or ionized calcium in these patients.

Adult↗
PubMed1996

Activation of c-myc gene mediates the mitogenic effects of oxalate in LLC-PK1 cells, a line of renal epithelial cells.

Recent studies on LLC-PK1 cells demonstrated that oxalate, a simple dicarboxylic acid, acts as a mitogen for these renal epithelial cells. Exposure to oxalate initiates DNA synthesis, induces the expression of one of the early growth response genes c-myc and stimulates proliferation of quiescent cultures of LLC-PK1 cells. The present studies examined the possibility that expression of the c-myc protooncogene is obligatory for this mitogenic response. Specifically we determined whether pretreatment with c-myc antisense oligonucleotides would block the proliferative effects of oxalate in LLC-PK1 cells. Quiescent cultures of LLC-PK1 cells were exposed to oxalate in the presence and absence of c-myc antisense and the effects of oxalate on c-myc protein expression (Myc), DNA synthesis and cell growth were assessed. Exposure of cells to oxalate alone increased the expression of Myc within two hours. Pretreatment with c-myc antisense abolished this response. Further, pretreatment of cells with c-myc antisense but not nonsense oligonucleotides blocked the oxalate-induced initiation of DNA synthesis. Increases in cell number in response to oxalate (measured after 72 hr exposure) were also blocked by exposure to c-myc antisense. These findings suggest that c-myc gene expression is critical for the mitogenic effects of oxalate in LLC-PK1 cells.

Animals↗