oxalates and Vitamin-B-Deficiency

Calculogenic potential of refined sugars galactose and fructose was examined in vitamin B6 deficient and control rats in terms of their capacity to increase urinary excretion of lithogens.. Male albino rats were fed vitamin B6 deficient diet with 51.7% sucrose+ starch or galactose or fructose as the source of carbohydrate. Pair-fed controls were maintained for all the groups for a period of four weeks. Twenty-four hour urine samples obtained at weekly intervals were analyzed for creatinine, calcium, oxalate, phosphate and uric acid. Microscopic urinalysis was performed at the end of the study.. Urinary calcium excretion increased with respect to baseline in all groups except vitamin B6 control group. On day 28, galactose and fructose-fed rats demonstrated significant hypercalciuria as compared to the sucrose + starch fed group. Vitamin B6 deficient rats (irrespective of the sugar fed) excreted significantly greater urinary calcium compared to pair-fed controls. Oxalate excretion was significantly increased in rats fed galactose compared to those fed fructose or sucrose + starch. Vitamin B6 deficiency further increased oxalate excretion by 1.5, 1.9 and 1.7 fold in sucrose + starch, fructose or galactose fed animals, respectively. Urinary uric acid excretion was enhanced only in fructose-fed rats. There was no change in urinary excretion of creatinine and phosphate in different experimental and control groups. Increased urinary saturation with lithogens caused pronounced crystalluria in all the vitamin B6 deficient groups as well as galactose control group.. The results suggest galactose ingestion is associated with a greater propensity to form calcium oxalate kidney stones than fructose. Calculogenic potential of galactose and fructose is further enhanced in vitamin B6 deficiency.

Topics: Animals; Calcium; Dietary Carbohydrates; Fructose; Galactose; Male; Oxalates; Phosphates; Photomicrography; Random Allocation; Rats; Rats, Wistar; Time Factors; Uric Acid; Urinary Calculi; Vitamin B Deficiency

The study was conducted to investigate the effect of vitamin A, B1 and B6 deficiency on oxalate metabolism in rats. A significant hyperoxaluria was the common observation in all the three vitamin deficiencies (vitamin B6 greater than vitamin A greater than vitamin B1). The activities of hepatic glycolate oxidase and glycolate dehydrogenase were markedly enhanced in vitamin-A- and vitamin-B6-deficient rats. However, lactate dehydrogenase levels remained unaltered in these deficiencies as compared to their respective pair-fed controls. Vitamin B1 deficiency of 4 weeks' duration could augment the activity of glycolate oxidase only, with no alterations in the glycolate dehydrogenase and lactate dehydrogenase levels. Intestinal oxalate uptake studies revealed increased bio-availability of oxalate from the gut in vitamin-A- and vitamin-B6-deficient rats. Thus, the results suggest the relative contribution of both exogenous as well as endogenous oxalate in the process of calculogenesis under various nutritional stress conditions in rat.

Topics: Animals; Male; Oxalates; Rats; Rats, Inbred Strains; Urinary Calculi; Vitamin A Deficiency; Vitamin B 6 Deficiency; Vitamin B Deficiency

According to the two-mutation model of neuroblastoma several investigations were performed in order to find the gene carrier in a family with familial neuroblastoma. The results of these former studies are as follows: 1. Neither chromosomal analyses of the peripheral blood nor the examinations of catecholamines nor of cystathionine in the urine could mark the first step to neuroblastoma. 2. Since cystathioniuria was not only seen in blood-relations but also in relatives by marriage and since vitamin B6 deficiency was revealed, cystathioninuria was interpreted as secondary to vitamin B6 deficiency. In this study the normal values of cystathioninuria and vitamin B6 supply were examined. Furthermore the effect of oral vitamin B6 loading on cystathioninuria and oxaluria in familial neuroblastoma was investigated and the vitamin B6 supply in the neighbours of the family was analysed. The results permitted the following conclusions: 1. In 46 of 58 children and adults cystathioninuria was found in an immeasurable range by column chromatography. Only in 12 persons it could be measured quantitatively. With the exception of 6 explanable elevations no value exceeded 20 mumol/24 hr. These results show that the acceptance of the limiting value of 20 mumol/24 hr for increased cystathioninuria is justified. 2. Vitamine B6 deficiency was found in two of 7 patients. In one child this could be explained by the underlying disease. This finding supports the suggestion that vitamine B6 deficiency can relative frequently observed. 3. The examinations of cystathioninuria and oxaluria before and after loading with vitamine B6 showed different results. Whereas oxaluria decreased after loading cystathioninuria was not surely influenced. 4. The neighbours of the members with familial neuroblastoma showed mostly a reduced vitamine B6 supply. This fact could be an indication of exogenous reason of vitamine B6 deficiency in familial neuroblastoma.

Topics: Adult; Child; Cystathionine; Female; Humans; Male; Mutation; Neuroblastoma; Oxalates; Pedigree; Pyridoxine; Vitamin B Deficiency

Topics: Animals; Avitaminosis; Biological Transport; Calcium Oxalate; Hematuria; Oxalates; Rats; Sulfathiazole; Sulfathiazoles; Vitamin B 6; Vitamin B Deficiency; Vitamins

Topics: Animals; Calculi; Cats; Kidney; Kidney Calculi; Nephrocalcinosis; Oxalates; Vitamin B 6 Deficiency; Vitamin B Deficiency; Vitamins