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.     

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.     

Role of Oxalobacter formigenes in preventing calcium oxalate kidney stones

Objective To screen Oxalobacter formigenes (OxF) from fresh feces of healthy adults, and study its effect on the the prevention of calcium oxalate kidney stones. Methods OxF was screened and cultured from fresh feces of healthy adults. The rat model of calcium oxalate stone was established by esophageal gavage of 0.8% of ethylene glycol. Rats were divided into a control group and four groups of rats with ethylene glycol-induced calcium oxalate kidney stones according to random number table. Three groups were treated with 106 CFU, 107 CFU, 108 CFU viable OxF every day, respectively, for 4 weeks. The blood and 24-hour urine samples were collected to detect the serum creatinine, urea nitrogen, serum and urine calcium, phosphorus, magnesium and urine oxalate every week. At the end of the 4th week, the rats were sacrificed and the kidney tissues were stained with HE and Yasue. The deposition and content of calcium oxalate crystals were observed under a light microscope. Results The bacteria strain isolated from fresh feces of healthy adults was 100% as same as the known ATCC35274 bacteria strain, which means the strain screened is OxF. Among the 5 groups, there were no significant differences in body weight, Scr, BUN, serum calcium, blood magnesium, blood phosphorus, urinary magnesium and urinary phosphorus. The 24-hour urinary calcium excretion in the model group was significantly lower than that of the control group (P＜0.05). After intervention with OxF solution, the 24-hour urinary calcium excretion in the 108 CFU OxF group was significantly higher than that in the model group (P＜0.05), while there was no significant difference between the other intervention groups and the model. The oxalic acid excretion of 106 CFU OxF group and 107 CFU OxF group was lower than that of the model, but the difference did not reach statistical significance (P＞0.05). The 24 h oxalic acid excretion in the 108 CFU OxF group was significantly lower than that of the model at the end of first week (P＜0.05), and continued to decrease for the next 3 weeks. After 4 weeks of intervention, no crystal formation was observed in the control group under the deflection microscope, but a large amount of calcium oxalate crystals were formed in the renal cortex and renal medulla. The crystals were piled up and connected to each other. Yasue staining coincided with the calcium oxalate crystal in the same part of the kidneys. Compared with the model, there was no significant change in the score of calcium oxalate crystal in the kidneys of 106 CFU OxF group and 107 CFU OxF group, while the score of calcium oxalate crystal in the kidneys of 108 CFU OxF group was significantly lower (P＜0.05). Conclusions OxF are successively screened from healthy adults. Daily administration of 108 CFU OxF can safely and effectively reduce the urinary oxalic acid excretion, prevent the formation of calcium oxalate crystals and inhibit the formation of stones in kidneys of rats.     

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.     

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.     

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.     

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.     

Dietary fibre: the effectiveness of a high bran intake in reducing renal calcium excretion

Summary Fifteen healthy women were given a standardized calcium-rich diet (1800 mg calcium/day) with or without 36 g bran for 5 days. A similar study was also carried out with rice, soy and wheat bran. Urine samples were also collected 24 h. With all brans renal calcium excretion decreased and renal oxalic acid excretion increased. However, influence of rice bran was statistically significant. After 5 days of consuming 36 g rice bran/day 14 of 15 subject showed decreased calcium excretion, but increased oxalic acid excretion. Relative supersaturation with calcium oxalate, as a measure for the risk of calcium stone formation, increased after addition of all brans.     

Effect of dietary calcium on stone forming propensity

PURPOSE: Epidemiological studies have reported that high calcium diet protects against kidney stone formation in normal subjects. This metabolic study was designed to elucidate the physiological and physicochemical effects conferring this apparent protection. MATERIALS AND METHODS: A total of 21 normal volunteers underwent 2 phases of study in a crossover, randomized design, wherein they consumed constant metabolic diets that matched the estimated highest and lowest quintiles of calcium intake from published epidemiological studies. RESULTS: Urinary calcium was significantly greater on the high calcium diet (148 +/- 55 versus 118 +/- 43 mg. daily, p <0.01, p <0.01) but urinary oxalate did not differ between diets. There was no difference in relative saturation ratio of calcium oxalate between the 2 diets. The high calcium diet significantly increased saturation of brushite and decreased that of uric acid. Due to the other differences between the diets (more fluid, potassium, magnesium and phosphate in the high calcium diet), the high calcium diet also increased 24-hour urinary volume, potassium, phosphorus, pH and citrate. After adjustment of these confounding variables, the high calcium diet significantly increased relative saturation ratio of calcium oxalate by 24%. CONCLUSIONS: High calcium diet from published epidemiological studies does not alter the propensity for calcium oxalate crystallization in normal subjects despite increased urinary calcium and unaltered urinary oxalate because of the greater amounts of ingested fluid, potassium and phosphate. However, high calcium intake alone, without concomitant changes in the diet, poses a modest risk for calcium stone formation.     

Effect of magnesium on calcium oxalate urolithiasis

Previous studies have shown that hypomagnesuria induced by magnesium deficient diet causes calcium oxalate crystal deposition in renal tubules of hyperoxaluric rats and administration of magnesium to these rats results in prevention of calcium oxalate crystallization in their kidneys. Based on these studies magnesium was claimed to be beneficial for calcium oxalate stone patients. However, hypomagnesuria is not a common phenomenon. To better understand the role of magnesium as an inhibitor of calcium oxalate crystallization in urine, we studied the effect of magnesium on calcium oxalate urolithiasis in rats on a regular diet and a hyperoxaluric protocol. Excess magnesium was administered to male rats on regular diet and a lithogenic protocol. Magnesium administration to hyperoxaluric rats did not result in significant changes in urinary excretion of calcium or oxalate or in calcium oxalate relative supersaturation. Urinary excretion of citrate was also not significantly altered. Some animals from both groups, those on magnesium therapy and those not on magnesium therapy had crystals deposited in their renal tubules. We conclude that excess magnesium has no significant effect on calcium oxalate urolithiasis in normomagnesuric conditions.     

Adequacy of a single stone risk analysis in the medical evaluation of urolithiasis

PURPOSE: We tested the hypothesis that a single 24-hour urine sample for stone risk analysis would be sufficient for the simplified medical evaluation of urolithiasis. MATERIALS AND METHODS: We retrospectively analyzed stone risk profile data on 24-hour urine samples obtained during random and restricted diets in 225 patients with recurrent urolithiasis. RESULTS: In 2 random samples we noted no significant difference in urinary calcium, oxalate, uric acid, citrate, pH, total volume, sodium, potassium, sulfate or phosphorus. For these risk factors there was a highly significant positive correlation in the 2 random samples (r > or = 0.68, p <0.0003) and the value of each was abnormal or normal in at least 81% of patients. Urinary magnesium and ammonium were significantly lower in random sample 2 than 1, the former by 4%. After calcium, sodium and oxalate dietary restriction mean urinary calcium and sodium plus or minus standard deviation decreased significantly by 25% from 251 +/- 125 to 187 +/- 98 mg. daily and by 38% from 183 +/- 87 to 113 +/- 57 mEq. daily, respectively. Other risk factors had a slight or no significant change. Correcting random urinary calcium for the excessive urinary excretion of sodium brought urinary calcium to 210 +/- 108 mg. daily, similar to the value on the restricted diet. CONCLUSIONS: The reproducibility of urinary stone risk factors is satisfactory in repeat urine samples. A single stone risk analysis is sufficient for the simplified medical evaluation of urolithiasis.     

The urinary response to an oral oxalate load in recurrent calcium stone formers

PURPOSE: Dietary oxalate may contribute up to 50% to 80% of the oxalate excreted in urine. We studied the urinary response to an oral oxalate load in male and female idiopathic recurrent calcium oxalate stone formers with and without mild hyperoxaluria to evaluate the potential pathophysiological significance of dietary oxalate. MATERIALS AND METHODS: A total of 60 recurrent calcium stone formers underwent an oral oxalate load test. Urine samples were obtained after an overnight fast. Each patient then received an oral oxalate load (5 mM. sodium oxalate dissolved in 250 ml. distilled water) and 3, 2-hour urine samples were obtained 2, 4 and 6 hours after the oxalate load. We compared the response to the oxalate load in patients with and without mild hyperoxaluria, and in male and female patients without hyperoxaluria. RESULTS: The peak urinary response occurred 4 hours after the oral oxalate load in all patients. Those with mild hyperoxaluria had a mean fasting urinary oxalate-to-creatinine ratio +/- SE of 0.027 +/- 0.003 and a mean peak urinary oxalate-to-creatinine ratio of 0.071 +/- 0.006. In comparison, patients with normal oxalate excretion had a fasting and peak urinary oxalate-to-creatinine ratio of 0.018 +/- 0.001 and 0.056 +/- 0.004, respectively (p <0.05). The mean 6-hour increment for urinary oxalate excretion after the oxalate load for patients with hyperoxaluria versus those with normal urinary oxalate excretion was 17.2 +/- 1.9 versus 12.1 +/- 0.98 mg. (p <0.05). In the subset of patients with normal urinary oxalate excretion mean 6-hour cumulative urinary oxalate excretion was 16.8 +/- 1.3 and 13.3 +/- 1.4 mg. in males and females, respectively (p not significant). CONCLUSIONS: Recurrent calcium stone formers with mild hyperoxaluria have higher fasting urinary oxalate and an exaggerated urinary response to an oral oxalate load compared with recurrent calcium stone formers with normal urinary oxalate excretion. Men and women stone formers without hyperoxaluria excrete similar fractions of an oral oxalate load. Increased gastrointestinal absorption and renal excretion of dietary oxalate may be a significant pathophysiological mechanism of stone formation in patients with mild hyperoxaluria.     

Effects of urinary prothrombin fragment 1 in the formation of calcium oxalate calculus

PURPOSE: We investigated the effects of urinary prothrombin fragment 1 in the formation of calcium oxalate urolithiasis. MATERIALS AND METHODS: Fresh urine and renal parenchyma from patients with calcium oxalate calculus and normal controls were collected. Urinary prothrombin fragment 1 was isolated and purified from urine. It was identified by sodium dodecyl sulfide-polyacrylamide gel electrophoresis and analysis of its first 13 N-amino acids. The inhibitory activity of urinary prothrombin fragment 1 on calcium oxalate crystal growth was tested by the seeded crystallization technique. Meanwhile, the gamma-carboxyglutamic acid composition of urinary prothrombin fragment 1 was analyzed by a previously described method and genetic mutation of the gamma-carboxyglutamic acid domain of urinary prothrombin fragment 1 from renal parenchyma was detected by polymerase chain reaction-single strand conformational polymorphism sequencing. RESULTS: The gamma-carboxyglutamic acid composition of urinary prothrombin fragment 1 was significantly decreased from normal (24.4 to 1.7 mol/1,000 amino acids) in patients with calcium oxalate calculus. The mean growth index +/- SD of urinary prothrombin fragment 1 to calcium oxalate crystals was 42.3 +/- 4.2 compared with the normal index of 19.2 +/- 2.8 (p <0.01). The polymerase chain reaction-single strand conformational polymorphism sequencing technique revealed no genetic mutation of the gamma-carboxyglutamic acid domain of urinary prothrombin fragment 1 in patients with calcium oxalate calculus. CONCLUSIONS: The gamma-carboxyglutamic acid composition of urinary prothrombin fragment 1 as well as its ability to inhibit calcium oxalate crystal growth was significantly decreased in patients with calcium oxalate calculus. This was not caused by genetic mutation of the gamma-carboxyglutamic acid domain of urinary prothrombin fragment 1. It is important to elucidate the mechanisms of calcium oxalate stones in view of urinary prothrombin fragment 1.     

Clinical studies of the recurrence of urolithiasis (3). Influence of sodium intake on urinary excretion of calcium, uric acid, oxalate, phosphate and magnesium

Relationship between urinary sodium excretion and urinary excretion of calcium, uric acid, oxalate, phosphate and magnesium was analyzed in 93 ambulatory patients with urolithiasis. There was a significant correlationship between urinary sodium excretion and urinary excretion of calcium, uric acid, oxalate (only in male stone formers), phosphate and magnesium, respectively. Under a salt restricted diet (NaCl 3-5 gm/day) for 3 days, urinary sodium excretion of 16 inpatients with urolithiasis was reduced remarkably together with significant reduction of urinary excretion of calcium, uric acid and oxalate. Urinary excretion of phosphate and magnesium showed no change. From these findings we conclude that restriction of sodium intake is an effective treatment for prevention of stone recurrence.     

Studies on crystalluria in calcium oxalate stone formers

Summary The excretion of calcium oxalate and calcium phosphate crystals was studied in fractionated 24 h urine from 7 men with recurrent calcium oxalate stone disease, both before and during daily administration of 5 mg bendroflumethiazide. Urinary calcium, oxalate, magnesium, citrate, phosphate, pH, and inhibition of calcium oxalate crystal growth rate were analyzed in all samples. Exclusively calcium oxalate crystals were found in 30 per cent of the samples, all with a pH below 6.25, whereas calcium phosphate was the crystal type encountered in urine with a pH above 6.50. Bendroflumethiazide decreased the volume of calcium phosphate but not of calcium oxalate crystals. During the period of observation there was no correlation between calcium oxalate supersaturation and calcium oxalate crystal volume, but a relationship was demonstrated between calcium phosphate supersaturation and calcium phosphate crystal volume.     

Reference range for gastrointestinal oxalate absorption measured with a standardized [13C2]oxalate absorption test

PURPOSE: Hyperoxaluria is a prominent risk factor for calcium oxalate urinary stones. Oxalate in urine is synthesized in the body or absorbed from food in the gastrointestinal tract. The amount of oxalate absorbed by patients with calcium oxalate stones may vary from a few percent to 50% of the dietary intake. Reference values for oxalate absorption measured under a standardized diet have never been attained in sufficient numbers from healthy individuals. Therefore, to our knowledge we collected for the first time the values required to interpret test results in patients with recurrent urinary stones. MATERIALS AND METHODS: A total of 120 healthy volunteers, including 60 females and 60 males, received an identical standard diet on 2 consecutive days. On the morning of day 2 a capsule containing 0.37 mmol. sodium [13C2]oxalate (not radioactive) was ingested with water. Urinary oxalate was measured by gas chromatography-mass spectrometry. Absorption at a fixed 800 mg. daily Ca input is expressed as a percent of the labeled oxalate dose.RESULTS: For the standardized [13C2]oxalate absorption test the reference range in 95% of the 120 volunteers was 2.2% to 18.5% (mean +/- SD 7.9% +/- 4.0%). The repeatability of the standardized test was determined in 26 of the 120 volunteers by repeating the test twice. The mean intra-individual SD was 3.39% +/- 1.68%. CONCLUSIONS: We assessed reference values of intestinal oxalate absorption using a standardized diet. Interindividual and intra-individual variance was high.     

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.     

Effects of magnesium citrate and phytin on reducing urinary calcium excretion in rats

Summary The aim of this study was to determine and compare the effects of both magnesium citrate and phytin on reducing urinary calcium excretion under high-calcium-diet conditions during single and combined treatments. An animal experiment was carried out over a period of 4 weeks in 35 male rats. Urinary calcium excretion was reduced significantly by magnesium citrate and/or phytin in rats fed on high-calcium diets. The hypocalciuric effect of magnesium citrate was more evident than that of phytin. Urinary magnesium excretion was high in all experimental groups. However, the urinary magnesium/calcium ratios showed a consistent increase only in the groups treated with magnesium citrate. Urinary citrate excretion showed a relative increase with the introduction of magnesium citrate plus phytin; however, in both the high-calcium-diet group and the magnesium-citrate group this was found to be reduced. Urinary phosphate excretion was slightly higher in the groups treated with phytin. There was no definite difference in urinary oxalate concentration between the groups. No significant change was noted in the serum concentration of calcium, magnesium, or phosphate.     

Oxalate synthesis from hydroxypyruvate in vitamin-B6-deficient rats

We studied the effects of an intravenous hydroxypyruvate load on endogenous oxalogenesis in rats receiving a standard diet or a vitamin-B6-deficient diet. Twelve male Wistar rats were randomized to two groups and were fed either a standard diet or a vitamin-B6-deficient diet for 3 weeks. Then the animals received an intravenous infusion of 100 mg/ml (960.6 μmol/ml) of hydroxypyruvate slowly over 10 min. Urine samples were collected just before hydroxypyruvate infusion and at hourly intervals until 5 h afterward. Urinary oxalate, glycolate, and citrate levels were measured by capillary electrophoresis. Hourly urinary oxalate excretion peaked within 2 h, while urinary glycolate excretion peaked at 1 h, after the hydroxypyruvate load in both control and vitamin-B6-deficient rats. Both urinary oxalate and glycolate excretion were higher in vitamin-B6-deficient rats than in control rats. Infusion of hydroxypyruvate increased the 5-h urinary oxalate and glycolate excretion to 0.68% (6.56 μmol) and 0.53% (5.10 μmol) of the administered dose (mol/mol), respectively, in the control rats, while oxalate and glycolate excretion, respectively, increased to 2.43% (23.36 μmol) and 0.79% (7.59 μmol) of the dose in the vitamin-B6-deficient rats. Urinary citrate excretion was significantly lower at baseline and all other times in the vitamin-B6-deficient rats than in the control rats. In conclusion, a hydroxypyruvate load increased endogenous oxalate synthesis in control rats, and its synthesis was even greater in vitamin-B6-deficient rats. Vitamin B6 deficiency also resulted in significant hypocitraturia.     

月见草油抑制草酸钙结晶形成的实验研究

目的了解月见草油在草酸钙结石形成中的作用,为临床治疗提供新的方法与思路。方法雄性SD大鼠60只,随机分为4组,各组15只。C组和D组以月见草油（含γ-亚麻酸9.2%）或葵花籽油（含亚油酸70%）10g/kg灌胃4周后,用诱石剂1%乙二醇（EG）加2%氯化氨喂饮,同时继续以月见草油或葵花籽油灌胃4周,8周后检测各组大鼠肾功能、24h血尿生化指标和肾草酸钙结晶情况;仅饲普通饲料（A组,空白组）和普通饲料加1%乙二醇（EG）加2%氯化氨喂饮（B组,成石组）大鼠作为对照。结果月见草油组肾组织水肿较轻,肾内草酸钙结晶数及肾成石率低于成石组（P〈0.05）,尿枸橼酸较成石组高（P〈0.01）,24h尿钙、尿草酸排泄均低于成石组（P〈0.01）,血尿素氮（P〈0.01）、血肌酐（P〈0.05）低于成石组。结论γ-亚麻酸能有效改善肾功能,减少尿钙及草酸的排泄,抑制实验鼠肾草酸钙结晶形成,在尿石症防治方面可能有一定应用价值。