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Query: UMLS:C0451641 (urolithiasis)
 3,973 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Studies in experimental animals showed that vitamin A deficiency enhanced the severity of urinary calculi disease. In India, children with low socioeconomic status are the major victims of bladder stone disease, and vitamin A deficiency is also more prevalent among these children. However, no systematic study is available to correlate the vitamin A-deficient status of children with their predisposition to urinary calculi disease. Vitamin A-deficient and normal boys were the subjects of this study. Twenty-four-hour samples of urine were collected from all the children at the beginning of the study and after normalizing the vitamin A status of the deficient children. Important risk factors were estimated in urine. Plasma vitamin A levels were also measured in these children. Among the deficient group, only children with plasma vitamin A levels of 15 micrograms and lower exhibited calcium oxalate crystalluria. Most importantly, abnormal crystalluria was observed in all children whose plasma vitamin A levels were 13 micrograms/dl or less. Compared to normal children the urine of vitamin A-deficient children showed the following changes: (a) reduced concentration of crystal growth inhibitors, namely citrate and glycosaminoglycans; (b) a decline in inhibitory activity toward calcium oxalate crystal growth; and (c) enhanced excretion of high risk factors, namely calcium and oxalate. Correction of vitamin A status normalized the above abnormal properties of urine. The results of this study strongly support the hypothesis that the vitamin A-deficient state is one of the factors that can enhance the risk of urolithiasis in susceptible populations.
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PMID:Contribution of vitamin A deficiency to calculogenic risk factors of urine: studies in children. 156 52

The effects of vitamin A deficiency on urolithiasis were investigated in male rats. A vitamin A-deficient diet caused important changes in the composition of the urine of the treated rats when compared with controls. One of the main effects was a decrease in the concentration of urinary glycosaminoglycans and zinc in the rats receiving the vitamin A-deficient diet. Significant differences were also found in plasma vitamin E and in the relation of vit E/vit A between treated and control groups but, in general, with no important differences in vitamin A. Nevertheless, significant differences in kidney content of vitamin A were observed between both groups. On the other hand, lesions of the cuboidal epithelium that covers the papillae in rats treated with the vitamin A-deficient diet were severe when compared with controls. The vitamin A and E plasma levels in urolithiasic humans were also investigated and compared with those found in a control group. No significant differences were observed in plasma vitamin A levels; nevertheless a significant increase in vitamin E and in the vit E/vit A ratio was clearly observed. These results could be related to a possible deficit of vitamin A in kidneys of stone formers, this being one of the diverse factors that can contribute to urolith development. Moreover, the deficit of important urinary crystallization inhibitors normally found in stone-formers, such as pyrophosphate and phytate, can also be related to the presence of low levels of renal vitamin A which prevents the enzymatic degradation of such inhibitors.
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PMID:Vitamin A and urolithiasis. 952 74

The early observations of Osborne, Mendel, and Ferry, and later of Higgins, showed that the incidence of urolithiasis was high in rats fed on diets deficient in fat soluble vitamins. Subsequently, the results of dark adaptation studies were interpreted as showing a relationship between vitamin A deficiency and calculous disease. However, a review of the literature including more recent data discloses that there is no evidence either clinical or experimental to support the claim that vitamin A deficiency is an etiologic factor in calculous disease in man in the United States.
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PMID:Vitamin A and urolithiasis; a review. 1316 Aug 18

Female Sprague-Dawley rats (n = 100; age, 3 wk) were fed diets that included a vitamin premix and either albumin or milk powder. Rats fed the albumin diet gained weight more slowly than did the other group. Between 19 and 28 wk of being fed the albumin diet, 12 rats died of bacterial cystitis and pyelonephritis. In addition, 2 more rats from the same dietary group developed peritonitis after ovariohysterectomy. Examination of the 44 rats fed the albumin diet that completed the 34-wk experiment revealed pyelonephritis in 68%, cystitis in 66%, urolithiasis in 27%, and nephrolithiasis in 5%. Squamous metaplasia of the transitional epithelium was present in all 44 rats, although other epithelia were histologically normal. Vitamin A deficiency was diagnosed after analyses of blood and liver samples. Analysis of the vitamin premix revealed approximately 25% of the expected amount of vitamin A. Because the milk powder contained sufficient vitamin A, deficiency did not occur in rats fed the milk powder diet. The major consequences of vitamin A deficiency in the rats were squamous metaplasia, bacterial infection, and calculus formation within the urinary tract. This report illustrates the importance of careful formulation and storage of vitamin premixes used in experimental diets. Vitamin A deficiency should be considered in rats with decreased weight gain and urinary tract disease even if ocular lesions are not present.
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PMID:Cystitis, pyelonephritis, and urolithiasis in rats accidentally fed a diet deficient in vitamin A. 1993 Aug 29