Search

We evaluated the metabolic and the nutritional aspects of 134 urolithiasis children in order to outline the characteristics of idiopathic urolithiasis in children. This prospective study group of 134 children (56 females, 78 males) with renal calculi was evaluated. The age range of the patients was six months to 16 years. A dietary survey was performed on every child. All patients were investigated with respect to stone localization and serum and urine risk factors. Statistical analysis of data was carried out using software SPSS 11.0 for Windows. Hypercalciuria was the most common risk factor detected in this group (28.3%). A decrease of water intake was noted in all age groups, especially in the rural area (549.6 mL/day vs. 1150.6 mL/day), and there was an increase in animal protein intake in 17 cases (mean: 1.9 g/kg). In addition, increased intake of starchy foods and food with high oxalate content (sorgum) were detected in the ten to 16 years age group (51%) of our study. Calcium oxalate monohydrate represents the principal component of idiopathic stone (58.2%), which is more frequent in children (68%) than in infants (51.7%) (P <0.02). The major etiology of idiopathic urolithiasis highlights the influence of dietary habit in stone formers in our country. The increased occurrence of calcium oxalate stones in school age children confirms the change in the etiology of urolithiasis according to age.

Objectives: To study the effect of a vitamin A supplemented diet on calcium-oxalate stone formation in rats and to test its expected action in the dissolution of renal calculi., Material and Methods: Twenty-four male Wistar rats were randomly divided into three groups of eight rats each. The first group (group A) received a normal diet for six weeks. The second group (group B) was fed a lithogenic diet by the addition of ethylene glycol 0.5% to drinking water for three weeks then a normal diet for three weeks. The third group (group C) received the same lithogenic diet for three weeks then a vitamin A supplemented diet 20 times the normal amount (5.1mg/100g of diet) at the three last weeks. One day before the end of treatment, each animal was placed for 24h in metabolic cage in order to collect urine samples and determine the urinary parameters., Results: The glomerular filtration rate and the urinary excretion of citric acid which fell in group B have been restored in group C., Conclusions: This study shows that a vitamin A supplemented diet at the rate of 20 times standard ration could improve the renal function by restoring the glomerular filtration rate and by increasing the urinary pH and excretion of citric acid., ((c) 2009 Elsevier GmbH. All rights reserved.)

Objective: To test whether increasing dietary calcium intake prevents calcium oxalate stone formation when the diet is oxalate-rich. Material and methods. Four groups, eight rats in each, were subjected to a lithogenic diet by the addition of 0.5% ethylene glycol to drinking water for 3 weeks. The first group, used as a control, simultaneously received a standard diet. The second group was supplemented with calcium at 500 mg/100 g of diet and the third group with oxalate at 3 g/100 g of diet. The diet given to the last group was supplemented with similar doses of calcium and oxalate. One day before the end of treatment, each animal was placed in a metabolic cage to collect 24-h urine samples and determine urinary parameters. The kidneys were removed to determine calcium oxalate deposits and for histological examination., Results: The number of calcium oxalate crystals in renal tissue was highest in the oxalate group and calcium oxalate deposits were also found to be elevated in this group. Hyperoxaluria and hypocitraturia, induced by a oxalate-rich diet, seemed to be the major causes contributing to aggravated renal stone formation. The protective effect of dietary calcium supplementation, which was clear in the calcium + oxalate group, was probably due to intestinal binding of oxalate by calcium, thereby reducing urinary oxalate excretion., Conclusion: Increased dietary calcium intake can prevent calcium oxalate stone formation only when the diet is oxalate-rich.

The aim of this study was to determine whether protein, administered alone or simultaneously with a hypercalcic diet, was able to aggravate calcium oxalate stone formation in rats. Thirty-two male Wistar rats were randomly divided into four groups of 8 rats each and assigned a calcium oxalate lithogenic diet added to their drinking water for 3 weeks. One group, used as reference, received a standard diet prepared in our laboratory. The second was assigned the same diet but supplemented with 7.5 g animal proteins/100 g diet. The third received a diet containing 500 mg calcium more than the standard group. The diet given to the last group was supplemented with calcium and protein at the same doses indicated previously. One day before the end of treatment, each animal was placed in a metabolic cage to collect 24-hour urine samples and determine urinary creatinine, urea, calcium, magnesium, phosphate, uric acid, citric acid and oxalate levels. Immediately thereafter, aortic blood was collected to determine the same parameters as in urine. The kidneys were also removed to determine calcium oxalate deposits. Our results showed an increased 24-hour urinary excretion of calcium, oxalate and uric acid and decreased urinary citric acid excretion only in groups that received protein supplementation. At the same time, calcium oxalate deposits were found significantly higher in hyperprotidic diets than reference or calcium-supplemented groups. According to these findings, glomerular filtration, fractional excretion of urea and reabsorption of water, calcium and magnesium were found significantly lower in hyperprotidic diets compared to other groups. These results demonstrate that proteins could seriously aggravate calcium oxalate stones and cause renal disturbances., (Copyright (c) 2005 S. Karger AG, Basel.)

The purpose of our study is to compare the status of vitamin A and E enters a group of male patients aged 30-40 years and having idiopathic lithiasis in the other whose origin of the lithiasis is awarded to a hypercalciuria and/or hypercalciuria and/or hyperoxaluria. Reference values were established from a normal subjects aged 30-40 years and having no history of nephrolithiasis. Our results showed that the mean levels of vitamin A was significantly lower in idiopathic renal stone-formers than metabolic stone-formers (p < 0.001). Compared to control group, the status of vitamin A was found lower only in idiopathic renal stone patients (p < 0.05). On the contrary, the mean levels of vitamin E were found similar in the two patient groups, but significantly lower compared to control group. These results suggested that idiopathic renal stone genesis could be generated by vitamin A deficiency.

Forty-eight Wistar rats were treated for 3 weeks with water containing 0.7% ethylene-glycol and divided into four groups. The first group, used as control, has received sodium chloride at 1 ml/100 g BW daily. The second group was intraperitoneally injected with selenium at 10 micrograms/d per 100 g BW as NaSeO3 for 3 weeks. The third group was intraperitoneally administered with 15 mg Vit E/d per 100 g BW as alpha-tocopherol acetate for 3 weeks. The last group was simultaneously administered vitamin E and Se at the same doses and periods as the precedent groups. One day before the end of the treatment, each animal was placed in a metabolic cage for collection of 24 h urine samples and determination of urinary creatinin, urea, calcium, magnesium, phosphate and oxalate levels. Immediately thereafter, all the rats were anesthetized and aortic blood was collected to determine the same parameters as in urine. The kidneys were also removed to determine calcium oxalate deposits, dry weight and to conduct a histological examination. Our results showed decreased ionic product and increased magnesium fractional reabsorption in the group receiving only selenium and in the group receiving selenium in combination with vitamin E, in comparison with the control animals. In view of the knowledge concerning the same protective action of Vit E and selenium, regardless of tubular membrane alteration, the absence of any inhibitory effect of Vit E on calcium oxalate formation suggests that selenium, like other minerals, could be stuck onto the crystal surface and would inhibit induction of new crystals, growth and aggregation.

Seventy two male Wistar-strain rats were fed lithogenic diet with ethylene-glycol within three weeks. At the end of this treatment, six rats were killed in order to determine the oxalate and calcium concentrations in renal tissue. Remained rats was randomly divided in four series, each series consisting of three groups. In first series (T), the animals were treated with distilled water; in the second (D1Zn), the animals were treated intramuscularly with the zinc at the rate of 24 micrograms per 100 grams of body weight and per day; in the third (D2Zn), 240 micrograms of zinc were administrated to animals and in the last series (D2Cu), the animals were treated at the same dose as the previous series, but with the copper. The groups which making up each series were killed successively at the 5th, 10th and 15th day after ending treatment with ethyleneglycol in order to determine urinary pH, percentage of water in renal tissue, uremia and concentrations of oxalate and calcium in renal tissue. Then, the comparisons of means were carried out, at each time, between different treated groups and reference group which was treated with distilled water. Litholytic effect was found in all series, including that which had been treated with distilled water. However, compared to reference animals, no acceleration of litholytic process was induced by zinc or copper. The high doses used in these experimentations proved therefore that calcium oxalate calculi were insoluble by zinc and copper.

Oxalate lithiasis was induced in control rats and rats previously given a vitamin A supplement for one week at the dose for 200 UI/d/kg body weight. Oxalate and calcium deposits in renal tissue measured 24 hours after the induction of lithiasis were found to be significantly lower in the vitamin A supplemented rats (p < 0.001 and p < 0.01) respectively). Renal function in these animals was also improved as compared with controls (p < 0.05). However, when vitamin A supplements were given for the same period and at the same dose, but after the induction of oxalate lithiasis, no difference regarding oxalate and calcium deposits was found between the two groups of animals. The same applied to renal function, which showed no improvement in the supplemented animals as compared with controls. These results suggest that vitamin A supplements have an inhibitory effect on lithogenesis but probably no litholytic action as such. The effect of vitamin A is probably related to its action on tubular cellular repair or an inhibitory effect on necrosis of these cells.

The addition of sucrose to drinking water of rats at the rate of 2.5 or 5 grams per 100 ml, for one month, induced hypercalciuria which appeared to be dependent on the degree of supplementation. In spite of these disorders, calcium deposits were not observed in treated animals. This protection against renal calculi was probably due to high urinary excretions of magnesium, phosphorus, zinc and copper. These lithogenesis inhibitors varied, like oxaluria and calciuria, in parallel with dietary sucrose intake.

Because of the diversity and importance of dietary factors in the pathogenesis of renal stones, a nutritional survey must be carried out in order to determine the quantity of protein, calcium, oxalate, sodium, sugar, vitamin D, vitamin C, ingested and the fluid intake and the quality of the drinking water. Although defects are observed in all parameters, it is essential to reduce the intake of protein, calcium, oxalate, sodium, vitamin D, vitamin C as well as increase the sucrose intake and recommend dietary therapy based on mineral water rich in bicarbonate.

Intraperitoneal injection of sodium oxalate, at the dose of 8 mg/100 g of body weight, induced into rats oxalate and calcium deposits in renal tissue, compared to animals which received distilled water (respectively P less than 0.05; P less than 0.05). However, when a zinc solution was administered previously, at the dose of 24 micrograms/100 g of body weight, oxalate and calcium accumulation was found to be significantly lower than in the group treated exclusively with sodium oxalate. Similar results were found when the metal used was copper, but oxalate accumulation was found to be significantly higher in this group than in the group treated with zinc (P less than 0.01). Compared to reference animals, which received distilled water, oxalate accumulation was found to be significantly decreased in the groups treated with both zinc (P less than 0.001) and copper (P less than 0.01), whereas calcium accumulation was found to be similar. Microscopic examination showed calcium crystals only in the group treated with sodium oxalate, preferentially localized in the renal papilla. These results suggest that zinc and copper, when administered at the dose of 24 mu/100 g of body weight, completely protect against experimental lithiasis induced by oxalic acid. However, the inhibitory effect of zinc was more pronounced than that of copper, especially against oxalate accumulation.

Sodium oxalate injected into young rats, via the intraperitoneal route, at a dose of 8 mg per 100 g of body weight, induced death in 50 p. cent of animals, and induced calcium oxalate crystals in renal tissue. When a zinc solution was administered prior to sodium oxalate, at the dose of 12 micrograms/100 g of body weight, the mortality rate decreased, and at the same time oxalate and calcium deposits were significant reduced (respectively P less than 0.01; P less than 0.01). The same results were found when zinc was administered at 24 micrograms/100 g of body weight, however, oxalic accumulation was found to be significantly lower in this group than in the group treated at 12 micrograms. This protection against calcium oxalate deposits was complete in the animals treated with various doses of zinc, because compared to reference animals, which received distilled water, calcium accumulation in these groups was not different and oxalate accumulation was also found to be lower (respectively P less than 0.05; P less than 0.001). Microscopic examination showed calcium crystals only in the group treated with sodium oxalate, localized preferentially in the renal papilla. All these experiments conclude on the total inhibitory effect of zinc on experimental lithiasis induced by oxalic acid, even though it was administered at a dose of only 12 micrograms/100 g of body weight.

Administration of ascorbic acid, at 150 mg/100 ml of water intake, for one month, induced hyperoxaluria in the rats (P less than 0.001) and decreased citraturia (P less than 0.001) magnesuria (P less than 0.001) and pyrophosphaturia (P less than 0.01). The same disorders were observed when the dose administered was 300 mg/100 ml, excepted that oxaluria was considerably enhanced in this group. Despite these variations, renal deposits were not observed, even in the animals receiving 300 mg of ascorbate/100 ml of water intake. This protection was due to decreased calcium excretion (P less than 0.01 in two groups) and probably to acidification of the urine.

Administration of high doses of vitamin D3 (2,600 IU/100 ml of drinking water) to adult rats, for one month, significantly altered renal function (P less than 0.01) and enhanced renal accumulation of oxalate (71.44 x 18.82 micrograms/g of tissue in treated rats vs 38.87 +/- 11.96 micrograms/g in untreated rats; P less than 0.001), phosphate (1.388 +/- 188 micrograms/g in treated rats vs 870 +/- 171 micrograms/g in untreated rats; P less than 0.01) and calcium (477 +/- 107 micrograms/g in treated rats vs 326 +/- 104 micrograms/g in untreated rats; P less than 0.01). Urinary analyses of principal promotors and inhibitors of lithogenesis revealed high calcium excretion (1,576 +/- 0.419 mg/24 hr in treated rats vs 0.969 +/- 0.214 mg/24 hr in untreated rats; p less than 0.01) and decreased magnesium excretion (0.330 +/- 0.135 mg/24 hr in treated rats vs 0.910 +/- 0.168 mg/24 hr in untreated rats; p less than 0.001). Microscopic calcium deposits were found in the medulla, especially in renal papilla. These results suggested that vitamin D3, when administered at high doses for a long time, may induce nephrocalcinosis and alter renal function.