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PubMed1998

Metabolic urinary correlates of calcium oxalate dihydrate in renal stones.

PURPOSE: We determined what metabolic features of the 24-hour urine predict calcium oxalate dihydrate in kidney stones. Prior studies have suggested that low urine magnesium, high urine calcium, high calcium-to-oxalate ratio and high urine supersaturation with respect to calcium oxalate monohydrate predict calcium oxalate dihydrate. MATERIALS AND METHODS: Stone analyses and results from 2, 24-hour pretreatment urine collections from 96 patients with nephrolithiasis were drawn from 3 kidney stone prevention centers. Standard stone risk measurements were made on the urine, including supersaturation for calcium oxalate monohydrate, brushite and uric acid. RESULTS: The main differences in metabolic urine findings were between patients with no calcium oxalate dihydrate and those with any calcium oxalate dihydrate in stones. Percent calcium oxalate dihydrate itself did not correlate with urine findings. Patients with no calcium oxalate dihydrate in stones showed a biphasic pattern of urine calcium oxalate monohydrate supersaturation, about half had values below almost any found among patients with calcium oxalate dihydrate in stones (less than 7) and the rest overlapped with the calcium oxalate dihydrate group. Except for higher calcium oxalate monohydrate supersaturation, patients with calcium oxalate dihydrate in stones had higher urine calcium excretion and lower urine citrate concentrations, even after calcium oxalate monohydrate supersaturation was considered. CONCLUSIONS: Patients with low calcium oxalate monohydrate supersaturation (less than 7) are unlikely to have calcium oxalate dihydrate in renal stones. However, many patients with no calcium oxalate dihydrate have higher calcium oxalate monohydrate supersaturation values, and so prediction of calcium oxalate dihydrate or its absence from urine findings is imperfect. Urine magnesium and the calcium-to-oxalate ratio are unrelated to calcium oxalate dihydrate.

Calcium Oxalate↗
PubMed1990

A further study of oxalate bioavailability in foods.

We extended the study of oxalate bioavailability by testing 7 additional food items: brewed tea, tea with milk, turnip greens, okra, peanuts and almonds. Nine normal subjects ingested a large serving of each of these items. The bioavailable oxalate was calculated from the increment in urinary oxalate during 8 hours after ingestion and bioavailability was determined as the percentage of total oxalate content in a given food item represented by bioavailable oxalate. Brewed tea and tea with milk, with a high oxalate content, had a low bioavailable oxalate level (1.17 and 0.44 mg. per load) because of the low oxalate availability (bioavailability of 0.08 and 0.03%). Turnip greens, with a satisfactory oxalate bioavailability (5.8%), had a negligible effect on urinary oxalate excretion, since oxalate content was relatively low (12 mg. per load). Okra, with a moderate oxalate content (264 mg. per load) had a negligible bioavailable oxalate (0.28 mg. per load). Only peanuts and almonds provided a moderate increase in oxalate excretion (3 to 5 mg. per load) due to the modest oxalate content (116 and 131 mg. per load) and oxalate bioavailability (3.8 and 2.8%). Thus, the ability of various oxalate-rich foods to augment urinary oxalate excretion depends not only on oxalate content but on the bioavailability.

Adult↗
PubMed1983

Complex pathogenesis of hyperoxaluria after jejunoileal bypass surgery. Oxalogenic substances in diet contribute to urinary oxalate.

Balance studies and oxalate loading tests were carried out in order to define the pathogenesis of hyperoxaluria in 8 patients with jejunoileal bypass surgery for severe obesity; two healthy volunteers were also studied. In the bypass patients, urinary oxalate was markedly elevated (118 +/- 43 mg/day, mean +/- SD) when they were on a high oxalate diet (252 mg/day). Hyperabsorption of dietary oxalate was confirmed by the markedly increased urinary recovery of [14C]oxalate given in a test meal. In addition, the oxalate radioactivity was excreted in urine far more slowly than in healthy volunteers, suggesting that the colon was a major site of oxalate absorption. Elevated urinary oxalate excretion persisted, averaging 38 +/- 12 mg/day, despite ingestion of a very low oxalate diet (approximately 6 mg/day), suggesting that the diet contained "oxalogenic" substances other than preformed dietary oxalate which also contributed to dietary oxalate in these patients. Urinary oxalate decreased in 7 of 8 patients, however, when protein-rich foods were removed from the diet, suggesting that at least one dietary factor was digestive products of protein or creatinine. These results confirm the current view that in patients with hyperoxaluria secondary to jejunoileal bypass, the majority of urinary oxalate derives from dietary oxalate that is absorbed from the colon. Tissue or bacterial production of oxalate or an oxalate precursor from dietary constituents associated with protein, however, also appears to contribute to urinary oxalate. The results provide an explanation for the reported difficulty of eliminating secondary hyperoxaluria by restriction of dietary oxalate alone.

Adult↗
PubMed2005

Urinary response to an oxalic acid load is influenced by the timing of calcium loading in rats.

PURPOSE: Dietary intake of calcium or dairy products has been shown to decrease urinary oxalate excretion by limiting its intestinal absorption. However, not enough attention has been given to whether there is any benefit from altering the schedule of ingesting calcium and oxalate. Therefore, we investigated the effects of changes in the timing of calcium and oxalate loading on urinary oxalate excretion. MATERIALS AND METHODS: Male Wistar rats weighing 180 to 200 gm were fasted and randomized into several groups. They were then administered normal saline or oxalic acid with or without calcium or milk. Calcium or milk was given immediately, or 5, 10, 15 or 30 minutes before or after the oxalate load. All treatments were given via gastrostomy. Urine samples were collected by bladder puncture just before administration and at hourly intervals up to 5 hours afterward. Urinary oxalate was measured by capillary electrophoresis. RESULTS: Urinary oxalate increased after the administration of oxalate alone, while it decreased when oxalate was combined with calcium or milk. Urinary oxalate showed a smaller increment when calcium or milk was given before than after oxalate loading, and it was much smaller when calcium or milk was given immediately before oxalate. CONCLUSIONS: Prior calcium loading appears to have a positive influence on decreasing oxalic acid absorption from the intestinal tract. Therefore, calcium or dairy products should always be ingested before a meal rich in oxalate to prevent oxalate absorption and decrease urinary oxalate excretion.

Analysis of Variance↗
PubMed1996

Characterization of oxalate transport by the human erythrocyte band 3 protein.

This paper describes characteristics of the transport of oxalate across the human erythrocyte membrane. Treatment of cells with low concentrations of H2DIDS (4,4'-diisothiocyanatostilbene-2,2'-disulfonate) inhibits Cl(-)-Cl- and oxalate-oxalate exchange to the same extent, suggesting that band 3 is the major transport pathway for oxalate. The kinetics of oxalate and Cl- self-exchange fluxes indicate that the two ions compete for a common transport site; the apparent Cl- affinity is two to three times higher than that of oxalate. The net exchange of oxalate for Cl-, in either direction, is accompanied by a flux of H+ with oxalate, as is also true of net Cl(-)-SO4(2-) exchange. The transport of oxalate, however, is much faster than that of SO4(2-) or other divalent anions. Oxalate influx into Cl(-)-containing cells has an extracellular pH optimum of approximately 5.5 at 0 degrees C. At extracellular pH below 5.5 (neutral intracellular pH), net Cl(-)-oxalate exchange is nearly as fast as Cl(-)-Cl- exchange. The rapid Cl(-)-oxalate exchange at acid extracellular pH is not likely to be a consequence of Cl- exchange for monovalent oxalate (HOOC-COO-; pKa = 4.2) because monocarboxylates of similar structure exchange for Cl- much more slowly than does oxalate. The activation energy of Cl(-)-oxalate exchange is about 35 kCal/mol at temperatures between 0 and 15 degrees C; the rapid oxalate influx is therefore not a consequence of a low activation energy. The protein phosphatase inhibitor okadaic acid has no detectable effect on oxalate self-exchange, in contrast to a recent finding in another laboratory (Baggio, B., L. Bordin, G. Clari, G. Gambaro, and V. Moret. 1993. Biochim. Biophys. Acta. 1148:157-160.); our data provide no evidence for physiological regulation of anion exchange in red cells.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1979

Renal elimination kinetics and plasma half-life of oxalate in man.

The renal handling of oxalate was studied by the injection of 14C-oxalate together with inulin as a glomerular marker into the renal artery in 6 patients. From the recovered amounts of the injected substances in the urine, time-concentration curves were constructed. Oxalate was excreted into urine 2.31 +/- 0.05 (SE) fold when compared to inulin. The maximal concentration of oxalate occurred at the same time as inulin, and there was no urinary precession of oxalate in comparison to inulin. From this part of the study we conclude that oxalate in addition to its filtered amount can probably enter the early part of nephron. In a second type of study, plasma levels of oxalate and inulin were observed over a period of 180 min, following intravenous injections in 7 volunteers. The decline of oxalate plasma concentrations followed first-order kinetics. Calculation of the rate constants of elimination assuming the 'one compartment open' model resulted in an oxalate to inulin ratio of 1.21 +/- 0.05. The oxalate half-life of elimination was 92 +/- 8 min, whereas that of inulin amounted to 112 +/- 9 min. The higher value of the calculated volume of distribution of oxalate compared to that of inulin indicates that oxalate enters a larger space than the extracellular fluid volume. The urinary recovery of intravenously injected oxalate was 97.2 +/- 1.4%, indicating that oxalate is excreted exclusively by the kidney. The observed differences of oxalate excretion, obtained with these two methods, could be attributed to the higher amount of ionized oxalate in the disequilibrium technique (rapid injections), entering the urine in a higher rate. Such a mechanism could explain the hyperoxaluria in calcium oxalate stone-forming patients.

Half-Life↗
PubMed2002

Calcium oxalate stone formation in genetic hypercalciuric stone-forming rats.

BACKGROUND: Over 54 generations, we have successfully bred a strain of rats that maximizes urinary calcium excretion. The rats now consistently excrete 8 to 10 times as much calcium as controls, uniformly form poorly crystalline calcium phosphate kidney stones, and are termed genetic hypercalciuric stone-forming (GHS) rats. These rats were used to test the hypothesis that increasing urinary oxalate excretion would not only increase the supersaturation with respect to the calcium oxalate solid phase, but also would increase the ratio of calcium oxalate-to-calcium phosphate supersaturation and result in calcium oxalate stone formation. METHODS: To increase urine oxalate excretion an oxalate precursor, hydroxyproline, was added to the diet of male GHS rats. The GHS rats were fed a standard 1.2% calcium diet alone or with 1%, 3% or 5% trans-4-hydroxy-l-proline (hydroxyproline). RESULTS: The addition of 1% hydroxyproline to the diet of GHS rats led to an increase in urinary oxalate excretion, which did not increase further with the provision of additional hydroxyproline. The addition of 1% and 3% hydroxyproline did not alter calcium excretion while the provision of 5% hydroxyproline led to a decrease in urine calcium excretion. The addition of 1% hydroxyproline led to an increase in urinary calcium oxalate supersaturation, which did not further increase with additional hydroxyproline. The addition of 1% and 3% hydroxyproline did not alter urinary supersaturation with respect to calcium hydrogen phosphate while the addition of 5% hydroxyproline tended to lower this supersaturation. Compared to rats fed the control and the 3% hydroxyproline diet the addition of 5% hydroxyproline increased the ratio of calcium oxalate supersaturation to calcium phosphate supersaturation. Virtually all rats formed stones. In the control and 1% hydroxyproline group, all of the stones were composed of calcium and phosphate (apatite), in the 3% hydroxyproline group the stones were a mixture of apatite and calcium oxalate, while in the 5% hydroxyproline group all of the stones were calcium oxalate. CONCLUSIONS: The provision of additional dietary hydroxyproline to GHS rats increases urinary oxalate excretion, calcium oxalate supersaturation and the ratio of calcium oxalate-to-calcium phosphate supersaturation, resulting in the formation of calcium oxalate kidney stones. Thus, with the addition of a common amino acid, the GHS rats now not only model the most common metabolic abnormality found in patients with nephrolithiasis, hypercalciuria, but form the most common type of kidney stone, calcium oxalate.

Animals↗
PubMed2001

The bioavailability of oxalate from Oca (Oxalis tuberosa).

PURPOSE: It is believed that soluble oxalate has higher bioavailability than insoluble oxalate. Oca (Oxalis tuberosa) is moderately high in oxalate and contains oxalate in soluble form only. We estimated the bioavailability of oxalate in oca based on the urinary excretion of oxalate after oxalate loading with oca to estimate the bioavailability of oxalate in oca. We also clarified whether bioavailability differs in various oxalate loads from the same food source and studied the effect of an additional calcium source on the bioavailability of oxalate from oca. MATERIALS AND METHODS: Four men and 4 women ingested 50, 100 and 150 gm. oca as well as 100 gm. oca with 100 gm. sour cream. Oxalate was measured in a 6-hour urine sample from each volunteer. RESULTS: The mean bioavailability of oxalate from oca plus or minus standard deviation was 1.44% +/- 1.31% during the 6-hour period after intake. There was no significant difference in oxalate bioavailability among oxalate intake levels in this study, although oca consumption with sour cream significantly decreased the uptake of oxalate (p <0.01). The variation in bioavailability among individuals was high in our study. CONCLUSIONS: The bioavailability of oxalate in oca appears to be similar to that in spinach. However, bioavailability varies among individuals and depends on other constituents of a combined meal.

Adult↗
PubMed2000

[Determinations of oxalate in urine and plasma by capillary electrophoresis].

PURPOSE: The determinations of oxalate in urine and plasma are important in the evaluation and treatment of patients with calcium oxalate nephrolithiasis. Although many analytical methods for determining oxalate have been developed, most of them need complicated sample preparation, and are expensive for routine examination. Especially for estimation of plasma oxalate, much more sensitive measurement is required because of the extremely low concentration. A simple and rapid assay for oxalate in urine and plasma by capillary electrophoresis has been described here, and utilized for assessment of renal oxalate clearance. In addition, simultaneous determination of urinary oxalate and citrate was developed. METHODS: A Waters Quanta 4000E system was used with a detection at 185 nm. Separation was obtained on a fused silica capillary, 60 cm long x 75 microns and 100 microns (i.d.) for urine and plasma samples respectively. Urine samples were diluted with 60 mM hydrochloric acid, and ultrafiltrates of plasma were acidified and diluted with 300 mM boric acid and 50 mM phosphoric acid. RESULTS: The intraassay coefficient variation was 2.7-4.0% for urinary oxalate, and 1.3-3.9% for citrate. The mean recovery ratio of 0.2 mM oxalate and 1.0 mM citrate added to 10 samples were 99.0% (92.6-107.4%) and 98.4% (91.2-103.9%), respectively. In the determination of plasma oxalate, the minimum detectable limit was 0.9 microM, the coefficient variation was 5.8-16.0%, and the recovery rate was 101.5% (87.8-125.6%). The plasma oxalate levels in 8 adult males were 2.39 +/- 1.46 microM (Mean +/- SD). Renal oxalate clearances with one hour method were 72.9 +/- 20.0 ml/min in 6 healthy controls and 83.2 +/- 27.8 ml/min in 8 stone formers. Oxalate/creatinine clearance ratios in each groups were 0.70 +/- 0.16 and 1.11 +/- 0.34 respectively. CONCLUSION: The simultaneous determination of urinary oxalate and citrate was satisfactory. Capillary electrophoresis is suited for routine examination of urinary oxalate and citrate with the advantage on simplicity and economy. The assay of plasma oxalate by this method was also acceptably sensitive, specific under a low temperature and an acidification.

Adult↗
PubMed1987

Dietary protein levels affect the excretion of oxalate and calcium in patients with absorptive hypercalciuria type II.

A total of 12 patients with absorptive hypercalciuria type II and 11 normal controls participated in a study to evaluate the effects of dietary protein levels on urinary calcium and oxalate excretion before and after a 1 gm. dose of oxalate. Two test periods were used during which calcium (less than 400 mg. per day) and oxalate were restricted. The first test was done under conditions of low dietary protein (12 per cent total caloric intake, 60 gm.) and the second test was done at a high protein level (25 per cent, 125 gm. protein). Twelve-hour urine specimens were obtained after dinner on day 3 of each diet (low and high protein) and again on day 4 when 1 gm. oxalate (spinach) was added to the dinner meal. The specimens were analyzed for calcium, oxalate and relative calcium oxalate saturation (concentration product ratio). There were no significant differences between the controls and subjects with absorptive hypercalciuria type II in oxalate excretion before the oxalate load on the low protein (controls 31.4 +/- 4.2 standard error, expressed as mmol. oxalate per mol. creatinine, and absorptive hypercalciuria type II 23.1 +/- 3.1) and high protein (controls 30.4 +/- 4.2 and absorptive hypercalciuria type II 28.8 +/- 5.9) diets. After the oxalate bolus the positive changes in oxalate excretion were 11.8 +/- 4.8 (low protein) and 17.8 +/- 4.7 (high protein) for controls, and 11.4 +/- 4.4 (low protein) and 31.8 +/- 5.2 (high protein) for patients with absorptive hypercalciuria type II. Thus, the increases in post-load urinary oxalate levels observed for controls and patients were greater on the high protein than on the low protein diets. After the oxalate load the increases in urinary oxalate and calcium oxalate supersaturation were significantly greater for patients with absorptive hypercalciuria type II than for control subjects for the high protein but not the low protein diets (p less than 0.05).

Adult↗
PubMed1995

Bony content of oxalate in patients with primary hyperoxaluria or oxalosis-unrelated renal failure.

Oxalate retention occurs in end-stage renal failure. Regular dialysis treatment does not prevent progressive accumulation of oxalate in cases of ESRF due to primary hyperoxaluria (PH), whereas such accumulation seldom seems to occur in oxalosis-unrelated ESRF. To elucidate this issue we have measured the bony content of oxalate on biopsies of the iliac crest taken from 32 uremic patients, 7 of them with ESRF associated with PH1 (6 cases) or PH2 (1 case). Ten subjects with normal renal function and no evidence of metabolic bone disease were taken as controls. Only trace amounts levels of oxalate were detected in normal subjects and oxalate to phosphate ratio was below 3:10,000. Non-PH dialyzed patients exhibited fivefold increases in oxalate levels, which rose to 5.1 +/- 3.6 mumol/g bony tissue. Calcium oxalate was estimated to represent 0.18% of the hydroxyapatite content of bone. Oxalate amounts were neither related to pre-dialysis plasma levels of oxalate, nor with duration of dialysis treatment, suggesting that accumulation was not progressive disorder. Oxalate levels were slightly higher in patients with a low turnover osteodystrophy compared to those with a high turnover pattern. Dialyzed patients with PH had remarkable increases in oxalate levels, which ranged between 14.8 and 907 mumol/g bony tissue. Oxalate deposition appeared to be progressive in that oxalate levels were significantly related to time on dialysis. In three patients calcium oxalate was a significant fraction of the mineralized bone. The occurrence of calcium oxalate crystals affected the histomorphometric patterns, that were featured by an increase in resorptive areas and a decrease in bone formation rate.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed2003

Milk and calcium prevent gastrointestinal absorption and urinary excretion of oxalate in rats.

Dietary oxalate plays a very important role in the formation of calcium oxalate stones, and dietary intake of calcium may decrease oxalate absorption and its subsequent urinary excretion. The purpose of the present study was to determine the effect on urinary oxalate excretion of an acute oral calcium load, standard milk, or high-calcium low-fat milk followed by a dose of oxalic acid. Male Wistar rats weighing 180-200 g were divided into 7 groups of 6 rats each. All animals were fasted for about 24 hours, anesthetized, and hydrated with normal saline at 3-4 mL/hour. Then the animals were given 1 mL of normal saline [Control], 10 mg (111.1 micromol) of oxalic acid [Ox alone], 2 mL of standard milk (calcium: 1.16 mg or 29 micromol/mL) [NCa milk], 2 mL of high-calcium low-fat milk (calcium: 2.05 mg or 51.3 micromol/mL) [HCa milk], equimolar calcium (4.44 mg or 111 micromol) followed by 10 mg of oxalic acid [Ca + Ox], 2 mL of high-calcium low-fat milk followed by 10 mg of oxalic acid [HCa milk + Ox], or 2 mL of standard milk followed by 10 mg of oxalic acid [NCa milk + Ox]. All treatments were administered via a gastrostomy. Urine samples were collected by bladder puncture just before administration and at hourly intervals up to 5 hours afterwards. Urinary oxalate was measured by capillary electrophoresis, while urinary calcium, magnesium and phosphorus were measured by inductively coupled plasma spectrometry. Urinary oxalate excretion peaked at 1 hour in the Ox alone group, while it peaked at 2 or 3 hours in the Ca + Ox, HCa milk + Ox, and NCa milk + Ox groups. Urinary oxalate excretion decreased significantly when 10 mg of oxalate was administered immediately after the administration of equimolar calcium, high-calcium low-fat milk, or standard milk. The cumulative urinary oxalate excretion over 5 hours was approximately 13.6%, 3.5%, 1.6%, and 2.4% in the Ox alone, Ca + Ox, HCa milk + Ox, and NCa milk + Ox groups, respectively. In conclusions, this study demonstrated that calcium salt, or dairy products containing calcium (especially high-calcium low-fat milk) could decrease the gastrointestinal absorption and subsequent urinary excretion of oxalate.

Animals↗
PubMed2000

Transport of oxalate across the rabbit papillary surface epithelium.

PURPOSE: The renal papilla and pelvic recesses of the mammalian kidney are thought to be the anatomical sites of initial kidney stone formation. We studied oxalate transport across the renal papillary surface epithelium. MATERIALS AND METHODS: In vitro oxalate transport across the papillary surface epithelium was studied by dissecting it off of the papilla and mounting it in a modified Ussing chamber. Experiments were conducted using physiological Ringer's solution at 37C. Removal or appearance of radioactive oxalate from the solution bathing the apical papillary surface epithelium surface was used as a measure of transepithelial transport. RESULTS: When only the papillary surface epithelium apical surface was exposed to oxalate (17 micromol./l.), the apical to basolateral flux of oxalate was 7.1 +/- 1.5 nmol./cm.2 per hour. When only the basolateral side was perfused with oxalate, the basolateral to apical oxalate flux was 1.6 +/- 0.7 nmol./cm.2 per hour. When the apical and basolateral surfaces were exposed to oxalate, a net apical to basolateral flux of oxalate was 3.0 +/- 0.7 nmol./cm.2 per hour. There was almost complete inhibition of apical to basolateral oxalate transport when the experiments were conducted at 20C. Absorption of oxalate across the papillary surface epithelium was decreased by the addition of 1 mM. 4, 4'-diisothiocyanatsostilbene-2,2'-disulphonic acid (DIDS), independent of sodium, but reduced by the presence of chloride in the apical solution. Increasing the pH of the apical solution from 7. 4 to 7.8 also resulted in a significant decrease in papillary surface epithelium oxalate uptake. CONCLUSIONS: Rabbit papillary surface epithelium demonstrates oxalate absorption by mechanisms that may be similar to those described previously for renal and colonic epithelia. Absorption of oxalate across the papillary surface epithelium may have a role in the prevention of initial calcium oxalate stone formation within the pelvic recesses.

Animals↗
PubMed2000

Impact of dietary calcium and oxalate ratio on urinary stone formation in rats.

BACKGROUND AND PURPOSE: Calcium interferes with oxalate absorption in the gut. We studied stone formation in rats fed diets containing various amounts of oxalate and calcium. MATERIALS AND METHODS: In one experiment, male Wistar rats were fed one of five experimental diets: basal diet (292 mM calcium + 8 mM oxalate) or basal diet plus either 100, 300, 500, or 1000 mM oxalate. In the other experiments, rats were given one of five diets: calcium-free diet alone or calcium-free diet plus 300 mM oxalate and either 0, 100, 200, or 300 mM calcium. Urine specimens were collected every week up to week 4. The kidneys were examined for stone formation and used for determination of tissue oxalate concentration by ion chromatography. Calcium and magnesium were measured by atomic absorption spectrophotometry. RESULTS: The higher the amount of oxalate in relation to calcium in the diet, the higher the urinary oxalate excretion. A low calcium level in the intestine enhanced the uptake of oxalate, leading to hyperoxaluria and calcium oxalate stone formation. CONCLUSION: The bioavailability of dietary oxalate in rats depends mainly on the relative intestinal calcium level. Hyperoxaluria without hyperabsorption of calcium could be induced by oral administration of a relatively high-oxalate and low-calcium (oxalate:calcium >1 [mol/mol]) diet. Exaggerated hyperabsorption of oxalate persists for several weeks and leads to calcium oxalate urolithiasis.

Animals↗
PubMed1984

Oxalate absorption and postprandial urine supersaturation in an experimental human model of absorptive hypercalciuria.

The effect of 1.25-dihydroxyvitamin D [1,25-(OH)2D] on dietary oxalate absorption and postprandial urine supersaturation with calcium oxalate was determined in 11 normal subjects. 1,25-(OH)2D increased the urinary excretion of orally administered [14C]oxalate in the 8 h period after a liquid meal containing 1.875 mmol of calcium and 0.83 mmol of oxalate (P less than 0.01), and during a 48 h period when the subjects ingested a diet containing 25 mmol of calcium and 3.3 mmol of oxalate/day (P less than 0.01); however, 1,25-(OH)2D administration had no effect on [14C]oxalate excretion when calcium was removed from the liquid meal. 1.25-(OH)2D increased 24 h urinary oxalate excretion from 28.7 +/- 2.1 mmol/mol of creatinine to 36.8 +/- 2.6 mmol/mol of creatinine (P less than 0.05) on the 10 mmol/day calcium diet and from 26.4 +/- 2.9 to 33.2 +/- 2.2 mmol/mol of creatinine (P less than 0.1) on the 25 mmol/day calcium diet. A linear correlation (r = 0.72) was found between plasma 1,25-(OH)2D levels and urinary [14C]oxalate excretion after the liquid meal. 1,25-(OH)2D administration produced postprandial supersaturation of urine with calcium oxalate and calcium oxalate crystalluria. These studies suggest that 1,25-(OH)2D increases oxalate absorption (and urinary excretion) by increasing calcium absorption, which results in less binding of calcium to oxalate in the intestine; therefore more oxalate is available for absorption. The combined effect of increased calcium and oxalate absorption results in postprandial supersaturation of urine with calcium oxalate, with resultant crystalluria.

Adult↗
PubMed2004

Adsorption of organic matter at mineral/water interfaces: 3. Implications of surface dissolution for adsorption of oxalate.

The adsorption of oxalate on a model aluminum oxide, corundum (alpha-Al2O3), has been examined over a broad range of oxalate concentrations (0.125-25.0 mM) and pH conditions (2-10). In situ attenuated total reflectance Fourier transform infrared (ATR-FTIR) measurements indicate that at low to intermediate concentrations ([oxalate] < or = 2.50 mM), oxalate adsorbs to corundum predominantly as a bidentate, mononuclear, inner-sphere complex involving both carboxyl groups. Significant contributions from outer-spherically bound oxalate and aqueous Ox(2-) are additionally observed at higher oxalate concentrations. Consistent with the ATR-FTIR findings, macroscopic adsorption data measured for oxalate concentrations of 0.125-2.50 mM can be generally well modeled with a single bidentate, inner-sphere oxalate complex using the charge distribution multisite complexation (CD-MUSIC) model. However, at intermediate oxalate concentrations (0.50 and 1.25 mM) and pH <5, the extent of oxalate adsorption measured experimentally is found to fall significantly below that predicted by CD-MUSIC simulations. The latter finding is interpreted in terms of competition for oxalate from dissolved Al(III), the formation of which is promoted by the dissolution-enhancing properties of the adsorbed oxalate anion. In accordance with this expectation, increasing concentrations of dissolved Al(III) in solution are found to significantly decrease the extent of oxalate adsorption on corundum under acidic pH conditions, presumably through promoting the formation of Al(III)-oxalate complexes with reduced affinities for the corundum surface compared with the uncomplexed oxalate anion.

Journal Article↗
PubMed1991

Oxalate binding to rat intestinal brush-border membrane in pyridoxine deficiency: a kinetic study.

Oxalate bound specifically to the intestinal brush-border membrane (BBM) of pyridoxine-deficient rats, but not to BBM of control rats. The binding of oxalate to intestinal BBM of pyridoxine-deficient rats was rapid, reversible, dependent on concentration of oxalate, temperature sensitive and competitively inhibited by oxalate analogues. Kinetic analysis of the oxalate binding data revealed induction of two distinct classes of receptor site for oxalate. The high-affinity oxalate binding sites, reached saturation at 60-70 nM oxalate, had a Kd of 24.29 nM and the number of binding sites were 30 pmoles (i.e., 1.8.10(13) molecules). The low-affinity oxalate binding sites, could not be saturated under experimental conditions upto 1 microM oxalate. It had a Kd of 487.5 nM and the number of binding sites were 156 pmoles (i.e., 9.4.10(13) molecules). The apparent energy of activation was 19 kcal/mol. The half-saturation concentration of inhibitor (IC50) of oxalate was 0.4.10(-5) M, while all other structural analogues of oxalate had higher IC50 values. Among the competitive inhibitors tested IC50 was in the following order, pyruvate greater than maleate greater than oxaloacetate greater than glyoxylate greater than parabonate greater than oxalate. These kinetic characteristics indicate involvement of a membrane protein in oxalate binding and transport in rat intestinal brush-border membrane in pyridoxine deficiency.

Alanine Transaminase↗
PubMed1993

The stomach: a new and powerful oxalate absorption site in man.

New information is provided regarding the site and nature of intestinal oxalate absorption in man. Intestinal absorption of oxalate was assessed indirectly from the increase in renal oxalate excretion following gastric administration of 5 mmol. oxalate loads. Four different types of loads have been used: sodium oxalate, sodium oxalate plus calcium gluconate, rhubarb and spinach. Studies were performed in 6 adult patients on permanent gastric tube feeding for various reasons. Gastric emptying was blocked by an intrapyloric balloon for the duration of the experiments and the gastric oxalate load was evacuated before the balloon was deflated. Under these conditions calcium oxalate was absorbed to the same extent as soluble oxalate. With increasing gastric loading time there is a linear increase in the urinary oxalate excretion: 15 to 21% of the gastric oxalate load appeared in the urine after 2 hours of loading, 24 to 45% after 4 hours and as much as 62% after 6 hours. These absorption kinetics and our experiment suggest that the stomach is not only just another oxalate absorption site but seems to be the critical site for intestinal oxalate absorption in an intact gastrointestinal tract. This finding opens a new field for the discussion of etiology and pathogenesis of calcium oxalate stone formation.

Aged↗