Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020438 (hypercalciuria)
 2,502 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Observed loss in body weight gain, increased lipid peroxidation reaction, decreased concentrations of antioxidants, ascorbic acid, alpha-tocopherol and reduced glutathione and antioxidant enzymes, glutathione peroxidase and catalase and increased concentration of hydroperoxides and hydroxyl radicals in vitamin B6 deficient rat liver [J Nutri Biochem, 2 (1991) 245] and kidney [Biochem International, 21 (1991) 599] were nearly normalized on feeding with vitamin E or methionine. Accumulation of oxalate and calcium during vitamin B6 deficiency was abolished by feeding vitamin E or methionine. Calcium oxalate deposition observed in vitamin B6 deficient kidney was completely prevented when fed along with vitamin E or methionine. However the hyperoxaluria and hypercalciuria persisted even after feeding with vitamin E or methionine.
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PMID:Restoration of tissue antioxidants and prevention of renal stone deposition in vitamin B6 deficient rats fed with vitamin E or methionine. 811 61

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.
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PMID:[Possible role of vitamin A and E deficiency in human idiopathic lithiasis]. 1295 18

The incidence of renal calculi has been evaluated to be 25% in urogenital tuberculosis patients. The stone could be caused due to the host, the pathogenic organism, or possibly by the treatment. Studies were carried out to find out the efficacy of vitamin E supplementation in reducing the risk of stone formation in renal tuberculosis patients. The study constituted four groups, Group I with 30 normal volunteers, the second group comprised of 36 renal tuberculosis patients (GuTb) a day before treatment. Third group comprised of 24 patients with regular anti tuberculosis drug regimen for sixty days. In the fourth group, 12 patients were treated with anti tuberculosis drug regimen along with supplementation of antioxidant vitamin E (200 mg/day) for sixty days. Hyperuricosuria and hypercalciuria were observed in group II and group III patients, along with increased excretion of oxalate and creatinine, accompanied by decreased excretion of inhibitors such as citrate and glycosaminoglycans (GAGs). Renal damage was evident with increased leakage of Lactate dehydrogenase (LDH), Alkaline phosphatase (ALP) and gamma-Glutamyl transferase (gamma-GT) in renal tuberculosis patients. From the results of the above study, it is obvious that increased urinary oxalate levels leads to cellular damage in GuTb patients, which is a prerequisite for crystal retention as revealed by the elevated urinary marker enzymes. Antioxidant therapy prevents membrane injury thereby reducing the risk of stone formation. Hence vitamin E supplementation has a salubrious effect in preventing stone forming tendency with routine anti tuberculosis drug regimen.
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PMID:Salubrious effect of vitamin E supplementation on renal stone forming risk factors in urogenital tuberculosis patients. 1528 96