Urinary oxalic acid excretion differs after oral loading of rats with various oxalate salts

BACKGROUND: To compare urinary oxalate excretion after the oral administration of oxalic acid, disodium oxalate, or calcium oxalate in rats. METHODS: Male Wistar rats were divided into four groups of six rats each and were intravenously hydrated with normal saline, and then were administered normal saline (control group), 10 mg of oxalic acid, equimolar disodium oxalate, or equimolar calcium oxalate via a gastrostomy. Urine specimens were collected just before administration and at hourly intervals up to 5 h afterwards. The urinary oxalate, calcium, magnesium and phosphorus levels were measured. RESULTS: Urinary oxalate excretion peaked at 1-2 h after administration of oxalic acid or equimolar disodium oxalate, while administration of calcium oxalate only caused a small increase of urinary oxalate excretion. Cumulative urinary oxalate excretion during 5 h was 1.69 +/- 0.10 mg (mean +/- SD; 17%), 1.43 +/- 0.13 mg (13%), and 0.22 +/- 0.03 mg (2%) after the administration of oxalic acid, disodium oxalate, and calcium oxalate, respectively. Urinary calcium excretion showed a decrease in the oxalic acid and disodium oxalate groups, while urinary magnesium or phosphorus excretion did not change significantly. CONCLUSION: The upper gastrointestinal tract seems to be the major site of oxalic acid absorption and only free oxalate is absorbed irrespective of whether it is the sodium salt or not. After binding to calcium in the gut, oxalic acid absorption seems to be inhibited in the presence of calcium and this means that calcium oxalate is poorly absorbed (at least in the upper gastrointestinal tract).     

Gastrointestinal oxalic acid absorption in calcium-treated rats

We studied whether urinary oxalate excretion after an acute oral load of oxalic acid is influenced by concomitant administration of calcium in rats. Male Wistar rats weighing approximately 180 g were divided into six groups of five animals each. After inducing anesthesia, the animals were orally (via a gastrostomy) given 110 μmol of oxalic acid along with 0, 27.5, 55, 110, or 220 μmol of calcium (0, 27.5, 55, 110, or 220 μmol Ca group, respectively). Saline was given to the control group instead of oxalic acid. Urine specimens were collected before administration and then at hourly intervals up to 5 h afterward. Urinary oxalate and citrate levels were measured by capillary electrophoresis, while urinary calcium, magnesium, and phosphorus levels were measured by ICP spectrophotometry. Urinary oxalate excretion peaked at 1 h after administration and was higher in the 0, 27.5, and 55 μmol Ca groups than in the control group. The urinary recovery of oxalate in these groups was 10–15%, while the recovery rate was less than 3% in other groups. Urinary Ca excretion showed no significant changes, either over time or between groups. Free oxalic acid is absorbed more readily from the gastrointestinal tract than calcium oxalate, while simultaneous administration of calcium appears to block intestinal oxalic acid absorption in a dose-dependent manner.     

Renal oxalate excretion following oral oxalate load in patients with urinary calculus disease and healthy controls

Oral oxalate loading using sodium oxalate or a vegetable juice was done to evaluate the intestinal absorption of exogenous oxalate in 30 patients with renal stones and 13 healthy controls. Fifteen calcium oxalate stone formers, 7 non-oxalate stone formers and 10 healthy volunteers were given an oral loading of sodium oxalate (500 mg). Urinary oxalate increased promptly, reaching a peak value within 4 to 8 hours after administration of a synthetic oxalate orally in a fasting state. In calcium oxalate stone formers, the mean increment of urinary oxalate and the bioavailability following oral sodium oxalate load were significantly higher than in the healthy controls and non-oxalate stone formers. Furthermore, intestinal hyperabsorption of oxalate in our criterion was defined in six patients with calcium oxalate stones (40%). On the other hand, eight calcium oxalate stone formers and three healthy controls were given vegetable juice. Urinary oxalate was increased only slightly after the ingestion, and there was no difference between calcium oxalate stone formers and normal controls. These results suggest that a certain hyperoxaluria might be induced by intestinal absorption of exogenous oxalate, and that the hyperabsorption might indicate a possible risk factor for calcium oxalate stone formation.     

Studies of dietary influence on urinary oxalate in calcium oxalate stone formers

In order to examine the effect of diet on the urinary excretion of oxalate, a spinach loading and milk loading experiment was performed in normal subjects and patients with single calcium oxalate stones and recurrent calcium oxalate stones after a rat experiment. When spinach (100 g, total oxalate 642.57 mg, insoluble oxalate 282.21 mg, taken oxalate 444.57 mg) was given with a low calcium diet to the patients, the increase of urinary oxalate was more prominent in those with recurrent stones; the mean urinary oxalate increased from 39.84 to 84.18 mg/day (P less than 0.01) in the group with recurrent stones, from 36.95 to 55.12 mg/day (P less than 0.05) in the group with single stones and from 33.99 to 42.78 mg/day in the control group. These increases in oxalate excretion could be ameliorated by the concurrent oral administration of milk (calcium 343 mg). Moreover, diurnal variation in oxalate excretion was observed. It was more evident under spinach load in the group with recurrent stones than in the control group. Urinary oxalate increased promptly, reaching peak levels between 4 and 6 hours after loading in the group with recurrent stones and single stones, and between 2 and 4 hours in the control group. The influence of the spinach load disappeared within 24 hours.     

Effects of calcium and magnesium on urinary oxalate excretion after oxalate loads

PURPOSE: Urinary oxalate is a primary determinant of the level of calcium oxalate saturation and the formation of calcium oxalate crystals, a key event in kidney stone formation. The primary objective of this study was to compare the effects of calcium carbonate and magnesium oxide on oxalate absorption. MATERIALS AND METHODS: An experimental model was used that allowed differentiation between endogenously and oxalate load-derived urinary oxalate. Twenty-four healthy subjects (10 males, 14 females) participated in three oxalate load (OL) tests: control (OL alone), calcium carbonate (OL with concomitant calcium carbonate ingestion), and magnesium oxide (OL with concomitant magnesium oxide ingestion). Oxalate loads consisted of 180 mg. unlabeled and 18 mg. 1,2[13C2] oxalic acid. Timed urine samples were collected after the OL for analysis of oxalate, calcium, magnesium, and creatinine. RESULTS: Both the calcium carbonate and magnesium oxide treatments were associated with significantly lower load-derived oxalate levels at all time points within the initial 24-hour post-oxalate ingestion period compared with levels observed for the control treatment. There were no treatment effects on endogenous oxalate levels. The efficiency of oxalate absorption for the calcium carbonate (5.1%) and magnesium oxide (7.6%) treatments was significantly lower than that for the control treatment (13.5%). CONCLUSIONS: The results suggested that magnesium was nearly as effective as calcium in reducing oxalate absorption and urinary excretion. Higher levels of urinary oxalate, calcium, and magnesium in males appeared to be largely a function of body size since gender differences either disappeared or were reversed when a correction was made for urinary creatinine excretion.     

Oxalate loading test for outpatients with calcium oxalate stones

A spinach loading experiment was performed on 9 normal subjects, 25 outpatients who were single calcium oxalate stone formers and 25 recurrent calcium oxalate stone formers. The experimental diet contained 445 mg of total oxalate, 163 mg of soluble oxalate and 115 mg of calcium. Urinary oxalate excretion was observed 2 hrs before and 6 hrs after the experimental diet was consumed. There was no significant difference in urinary oxalate excretion in preloading urine of normal subjects and stone formers. However, urinary oxalate excretion in postloading urine was significantly elevated in stone formers. This loading test is recommended as a simple and valuable screening method of hyperabsorption of oxalate on outpatients with calcium oxalate stones.     

The determination of urinary oxalate by gas chromatography

A new quantitative determination method for urinary oxalate by gas chromatography has been established. This method consists of concentration of urine to dryness followed by methylation of the oxalic acid with 7 per cent hydrochloric acid-methanol, subsequent extraction with chloroform and gas chromatographic analysis. The advantages of the technique are smaller sample sizes (only 5 ml.), rapidity (within 2 to 3 hours) and accuracy (99.14 plus or minus 1.34 per cent recovery). In addition, the treatment of the sample is simple and no specialized equipment is required. Therefore, this method is recommended to clinicians for routine determination of oxalic acid in urine. Urinary oxalate content was analyzed with this method in 62 male patients with calcium oxalate stones. Urinary oxalate concentration and excretion in 33 patients with recurrent stones were significantly higher than in the 22 controls using Welch's test.     

Effect of ethyl icosapentate on urinary calcium and oxalate excretion

BACKGROUND: The effect of ethyl icosapentate (EPA-E) on urinary calcium and oxalic acid excretion was examined to evaluate whether EPA-E is useful in the prevention of calcium-containing urinary stones. METHODS: For 6 months, urine was measured daily from 40 calcium-containing urinary stone producers at an outpatient clinic, before and after the administration of 1800 mg/day EPA-E. The urine was measured for volume, urea nitrogen, creatinine, calcium, magnesium, phosphorus, uric acid, oxalic acid and citric acid. Serum total cholesterol and triglyceride were also measured. RESULTS: Urinary calcium excretion was not reduced in any of the patients or particular hypercalciuric groups, nor did the level of calcium change. However, nine of the 25 hypercalciuric patients experienced a significant urinary calcium reduction to the normal calciuric level (a reduction of approximately 44%). It is not known why these particular patients experienced a reduction. Urinary oxalic acid did not change, whether hypercalciuria was present or not. CONCLUSIONS: These findings suggest that EPA-E is not particularly effective in reducing urinary calcium excretion in the hypercalciuric patients, but it needs future investigation because some patients experienced significant urinary calcium reduction.     

Intestinal absorption of oxalate and calcium in patients with jejunoileal bypass

Jejunoileal bypass (JIB) has been widely performed for treatment of excessive obesity. Formation of calcium oxalate stones is a common side effect. Since, under physiological conditions, the intestinal absorption of calcium and that of oxalate are interrelated, intestinal oxalate and calcium absorption were measured in the present study by isotope techniques in 19 JIB patients and 20 healthy controls. The JIB patients showed pronounced hyperoxaluria and markedly increased absorption of oxalate, with a urinary excretion of 14C-oxalate of 29 +/- 19% (controls 6.2 +/- 3.7%; p less than 0.001). There was a strong correlation between the intestinal absorption and urinary excretion of oxalate in the JIB patients (r = 0.72; p less than 0.001). Furthermore, their oxalate kinetics was altered, with continued urinary excretion of 14C-oxalate for up to 48 hours. The JIB patients also had reduced calcium absorption (36 +/- 9.1% vs. 47 +/- 9.0%; p less than 0.001) and patients with malabsorption of calcium and low urinary calcium had the highest intestinal absorption and urinary excretion of oxalate. It is concluded that hyperoxaluria in JIB patients is due to a significant extent to hyperabsorption of oxalate.     

Dietary oxalate loads and renal oxalate handling

PURPOSE: Dietary oxalate makes a significant contribution to urinary oxalate excretion and, thus, may have a role in calcium oxalate kidney stone formation. Studies have indicated that the ingestion of oxalate rich foods results in transient increases in plasma oxalate concentrations and urinary oxalate excretion. We examined changes in plasma and urinary oxalate following oral crystalline oxalate loading under controlled dietary conditions to further define the renal handling of oxalate by normal adults. MATERIALS AND METHODS: Six normal adult subjects consumed controlled diets of known oxalate content for 1 week before ingesting loads of 0, 2, 4 and 8 mmol of oxalate. Urinary and plasma changes were measured to assess renal oxalate handling. Urinary excretion of proximal tubule derived enzymes and isoprostanes was monitored to assess for renal injury and oxidative stress. RESULTS: Time and dose dependent changes in plasma oxalate, urinary oxalate and in the clearance ratio of oxalate-to-creatinine were observed. A significant correlation (r=0.43, p <0.001) between the oxalate-to-creatinine clearance ratio and plasma oxalate levels was identified. No changes in urinary markers of oxidative stress or renal injury were observed following the 8 mmol oxalate load. CONCLUSIONS: Oxalate is rapidly absorbed and cleared by the kidney by filtration and secretion following an oral oxalate load. Renal oxalate secretion has a significant role in the renal handling of an oral oxalate load. There is no evidence of acute renal injury or oxidative stress with oral oxalate loads in these experimental conditions.     

13C2]oxalate absorption in children with idiopathic calcium oxalate urolithiasis or primary hyperoxaluria

Intestinal oxalate absorption is an important part of oxalate metabolism influencing its urinary excretion and its measurement can be a valuable diagnostic tool in hyperoxaluric disorders. In this study, we use [(13)C(2)]oxalate absorption under standardized dietary conditions to assess intestinal oxalate absorption and its impact on urinary oxalate excretion. Tests were conducted in age-matched pediatric patients that included 60 with idiopathic calcium oxalate urolithiasis, 13 with primary hyperoxaluria, and 35 healthy children. In the idiopathic stone formers, median oxalate absorption was significantly higher than that in the controls or in patients with primary disease. From standardized values obtained in control patients, oxalate hyperabsorption was detected in 23 patients with idiopathic disease but not in any patients with primary hyperoxaluria; therefore, a significant correlation between intestinal absorption and urinary excretion was found only in those with the idiopathic disease. We have shown that increased intestinal oxalate absorption is an important risk factor of idiopathic calcium oxalate urolithiasis. In contrast, low intestinal oxalate absorption in patients with primary hyperoxaluria indicates that only foods with excessive oxalate content be restricted from their diet.     

Transient hyperoxaluria after ingestion of chocolate as a high risk factor for calcium oxalate calculi

In 6 male subjects the diurnal variation of urinary oxalic acid excretion was studied after ingestion of chocolate, a food stuff rich in oxalic acid. The ingestion of chocolate caused a striking but transient increase in urinary oxalic acid excretion due to its absorption in the upper gastrointestinal tract. The peak excretion rates occurred 2-4 h after the intake of the chocolate. The peak values were 235% of the fasting excretion rate in the trial with 50 g chocolate and 289% in the trial with 100 g chocolate and reached the amounts found in cases with primary hyperoxaluria. The administration of ranitidine had no influence on oxalic acid absorption. The transient hyperoxaluria observed seems to be an important factor for the formation of calcium oxalate calculi in patients on risk for stone disorders.     

Intestinal and renal handling of oxalate loads in normal individuals and stone formers

The renal handling and intestinal absorption of dietary oxalate are believed to be risk factors for calcium oxalate stone formation. In this study, we have examined the time and dose effects of soluble oxalate loads on the intestinal absorption and renal handling of oxalate in six stone formers (SF) and six normal individuals (N) who consumed diets controlled in oxalate and other nutrients. Urinary and plasma oxalate changes were monitored over 24 h after ingestion of 0, 2, 4, and 8 mmole oxalate loads, containing a mixture of ¹²C- and ¹³C₂-oxalate. There were significant time and dose dependent changes in urinary oxalate excretion and secretion after these loads. However, there were no significant differences between SF and N in both the intestinal absorption and the renal handling of oxalate loads, as measured by the urinary excretion of oxalate (P = 0.96) and the ratio of oxalate to creatinine clearance (P = 0.34). ¹³C₂-oxalate absorption studies showed three of the subjects, two SF and one N, had enhanced absorption with the 8 mmole load. A clear difference in absorption was demonstrated in these individuals during the 8–24 h interval, suggesting that in these individuals there was greater oxalate absorption in the large intestine as compared to the other subjects. This enhanced absorption of oxalate warrants further characterization. This research was supported in part by NIH grants RO1 DK62284 and MO1 RR07122.     

Endogenous oxalogenesis after acute intravenous loading with ethylene glycol or glycine in rats receiving standard and vitamin B6‐deficient diets

Objectives: The effect on endogenous oxalate synthesis of acute intravenous loading with ethylene glycol or glycine was investigated in rats on a standard or a vitamin B6‐deficient diet. Methods: Twenty‐four male Wistar rats weighing approximately 180 g were randomly divided into ethylene glycol and glycine groups of 12 animals each. These groups were further divided into two subgroups of six animals each that were fed either a standard or a vitamin B6‐deficient diet for 3 weeks. Animals of these two subgroups received an intravenous infusion of 20 mg (322.22 µmol) of ethylene glycol or 100 mg (1332.09 µmol) of glycine, respectively. Urine samples were collected just before intravenous infusion of each substance and at hourly intervals until 5 h after receiving the infusion. Urinary oxalate, glycolate, and citrate levels were measured by capillary electrophoresis. Results: Urinary oxalate and glycolate excretion was significantly increased after ethylene glycol administration. Significant differences between the control and vitamin B6‐deficient groups were found. In contrast, there were only small changes of oxalate and glycolate excretion after glycine administration. Recovery of the given dose of ethylene glycol as oxalate in 5‐h urine was 0.31% and 7.15% in the control and vitamin B6‐deficient groups, respectively, whereas recovery of glycolate was 0.68% and 7.22%, respectively. Conclusions: Ethylene glycol loading has a significant effect on urinary oxalate excretion in both normal and vitamin B6‐deficient rats, whereas glycine loading only has a small effect. Oxalate and glycolate excretion after ethylene glycol loading were respectively 23‐fold and 11‐fold higher in vitamin B6‐deficient rats than in controls.     

Urine composition following jejunoileal bypass

The urinary excretion of oxalate, calcium, citrate, magnesium, urate and creatinine and the inhibition of calcium oxalate crystal growth were determined in 30 patients operated with three different types of jejunoileal bypass. In addition the ion-activity products of calcium oxalate and calcium oxalate saturation were calculated. 15 of the patients had formed urolithiasis postoperatively. The patients were investigated on an out-patient basis with their ordinary diet. All patients had hyperoxaluria. The oxalate excretion did not seem to decrease with time after operation. The patients operated with a biliointestinal shunt had a significantly higher excretion of oxalate than those with the other two types of operation, indicating that variations in the anatomy of the small intestine after jejunoileal bypass might result in different absorption of oxalate or oxalate precursors. Urinary oxalate, calcium oxalate saturation and ion-activity products were higher whereas the excretion of calcium, magnesium and citrate was lower in patients than in controls. The urine volumes, excretion of creatinine and urate and inhibition of calcium oxalate crystal growth were equal in patients and controls. Analogous urine composition was found in patients both with and without urolithiasis with the exception of a higher magnesium excretion observed in stone formers.     

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.     

Use of a probiotic to decrease enteric hyperoxaluria

BACKGROUND: Patients with inflammatory bowel disease have a 10- to 100-fold increased risk of nephrolithiasis, with enteric hyperoxaluria being the major risk factor for these and other patients with fat malabsorptive states. Endogenous components of the intestinal microflora can potentially limit dietary oxalate absorption. METHODS: Ten patients were studied with chronic fat malabsorption, calcium oxalate stones, and hyperoxaluria thought to be caused by jejunoileal bypass (1) and Roux-en-Y gastric bypass surgery for obesity (4), dumping syndrome secondary to gastrectomy (2), celiac sprue (1), chronic pancreatitis (1), and ulcerative colitis in remission (1). For 3 months, patients received increasing doses of a lactic acid bacteria mixture (Oxadrop), VSL Pharmaceuticals), followed by a washout month. Twenty-four-hour urine collections were performed at baseline and after each month. RESULTS: Mean urinary oxalate excretion fell by 19% after 1 month (1 dose per day, P < 0.05), and oxalate excretion remained reduced by 24% during the second month (2 doses per day, P < 0.05). During the third month on 3 doses per day oxalate excretion increased slightly, so that the mean was close to the baseline established off treatment. Urinary oxalate again fell 20% from baseline during the washout period. Calcium oxalate supersaturation was reduced while on Oxadrop, largely due to the decrease in oxalate excretion, although mean changes did not reach statistical significance. CONCLUSION: Manipulation of gastrointestinal (GI) flora can influence urinary oxalate excretion to reduce urinary supersaturation levels. These changes could have a salutary effect on stone formation rates. Further studies will be needed to establish the optimal dosing regimen.     

Physicochemical metabolic characteristics for calcium oxalate stone formation in patients with gouty diathesis

PURPOSE: We determined why calcium oxalate stones instead of uric acid stones form in some patients with gouty diathesis. MATERIALS AND METHODS: Gouty diathesis was diagnosed from absence of secondary causes of uric acid stones or low urinary pH, and reduced fractional excretion of urate with discriminant score of the relationship between urinary pH and fractional excretion of urate less than 80. From the stone registry 163 patients with gouty diathesis were identified, including 62 with uric acid stones (GD + UA) and 101 patients with calcium oxalate stones (GD + Ca). Metabolic data and 24-hour urinary chemistry study were compared between the 2 groups. RESULTS: Compared with GD + UA, GD + Ca had significantly greater urinary calcium (196 +/- 96 mg per day vs 162 +/- 82 mg per day, p <0.05) and significantly lower urinary citrate (430 +/- 228 vs 519 +/- 288 mg per day, p <0.05), resulting in higher urinary saturation of calcium oxalate. Both groups had low urinary pH (less than 5.5) and high urinary undissociated uric acid (greater than 100 mg/dl). Urinary calcium post-oral calcium load was significantly higher in GD + Ca than in GD + UA (0.227 vs 0.168 mg/dl glomerular filtrate, p <0.001). CONCLUSIONS: Calcium oxalate stones may form in some patients with gouty diathesis due to increased urinary excretion of calcium and reduced excretion of citrate. Relative hypercalciuria in GD + Ca may be due to intestinal hyperabsorption of calcium.     

Association of absence of intestinal oxalate degrading bacteria with urinary calcium oxalate stone formation

AIM: Urinary concentration of oxalate is considered an important factor in the formation of renal stones. Dietary oxalate is a major contributor to urinary oxalate excretion in most individuals. Furthermore, oxalate degrading bacteria have been isolated from human feces. We investigated the significance of oxalate degrading bacteria for urinary oxalate excretion and urinary stone formation. METHODS: Twenty-two known calcium oxalate stone-forming patients (stone formers) and 34 healthy volunteers (non-stone formers) were included in the study. Stool specimens were inoculated into pepton yeast glucose (PYG) medium supplemented with oxalate under anaerobic condition at 37 C for one week. After the incubation period, each colony was checked for the loss of oxalate from the culture medium. A 24-h urine sample was collected in 43 individuals and analyzed for oxalate excretion. RESULTS: Twenty-eight of 34 (82%) healthy volunteers and 10 of 22 (45%) calcium oxalate stone formers were colonized with oxalate degrading bacteria. Calcium oxalate stone formers were more frequently free of oxalate degrading bacteria (P < 0.01). Urinary excretion of oxalate in those with oxalate degrading bacteria was significantly less than in those without oxalate degrading bacteria (P < 0.05). Hyperoxaluria (> 40 mg/day) was found in four of 27 individuals (15%) with oxalate degrading bacteria compared to seven of 16 (44%) without oxalate degrading bacteria (P < 0.05), suggesting an association between the absence of oxalate degrading bacteria and the presence of hyperoxaluria. CONCLUSION: The absence of oxalate degrading bacteria in the gut could promote the absorption of oxalate, thereby increasing the level of urinary oxalate excretion. The absence of oxalate degrading bacteria from the gut appears to be a risk factor for the presence of absorptive hyperoxaluria and an increased likelihood of urolithiasis.     

Association of dietary fatty acids with urinary oxalate excretion in calcium oxalate stone-formers in their fourth decade

OBJECTIVE: To examine the influence of the dietary intake of fatty acid on urinary oxalate excretion in calcium oxalate stone-formers in their fourth decade, as previous reports show that animal fat intake is associated with urinary oxalate excretion. PATIENTS AND METHODS: The dietary intake of 58 idiopathic stone-formers in their fourth decade was recorded using the dietary-record method. The patients collected 24-h urine samples at home and their urinary oxalate excretion was measured in a clinical biochemistry laboratory. The results were used to determine the relationship between the dietary intake of fatty acids and urinary oxalate excretion. Associations between urinary oxalate excretion and dietary contents of animal fat, animal protein and various fatty acids were assessed using Spearman's correlation coefficient and multiple regression. RESULTS: The dietary content of arachidonic acid was positively correlated with urinary oxalate excretion, as assessed by univariate and multivariate analysis. CONCLUSION: The association between arachidonic acid and oxalate excretion suggests that arachidonic acid increases the intestinal absorption of oxalate and increases the clearance of oxalate in the kidneys.