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Query: UMLS:C0020500 (hyperoxaluria)
 912 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Clinical studies suggest that steatorrhoea can be associated with excessive absorption of dietary oxalate. We examined the influence of bile salts, Ca++, and long-chain fatty acid on the absorption of oxalate and water by rat intestine in vivo. Absorption was measured under steady-state conditions during single-pass infusions. Each intestinal segment served as its own control. In jejunum, 10 mM taurocholate, the principal salt in rat bile, depressed absorption of oxalate and water. Absorption was not depressed further by Ca++ or linoleic acid. In ileum, 10 mM taurocholate did not inhibit absorption. Linoleic acid, 2 mM, depressed absorption of both oxalate and water. In colon 10 mM taurocholate decreased absorption. Net water transport was depressed further when linoleic acid was added to the infusion, but oxalate absorption was enhanced. Ca++ negated these effects of linoleic acid. It is concluded that long-chain fatty acids may enhance the absorption of oxalate from the rat colon. This observation may be relevant to understanding hyperoxaluria in patients with steatorrhoea.
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PMID:Regional differences in oxalate absorption by rat intestine: evidence for excessive absorption by the colon in steatorrhoea. 115 92

These studies were designed to evaluate the effect of bile salts and fatty acids on colonic oxalate absorption. Five millimolar deoxycholate significantly increased oxalate absorption from 34.2 +/- 9.4 nmoles per min per g dry weight to 330.4 +/- 47.3 (P less than 0.001) and changed water absorption to water secretion. Deoxycholate also increased the absorption of urea, decreased the electrical potential difference, and increased colonic clearance of oxalate, observations which are consistent with an increase in colonic mucosal permeability. In contrast, taurocholate did not increase oxalate absorption. Ricinoleic acid also significantly increased the absorption. These results suggest that bile salts and fatty acids increase colonic absorption of oxalate. Oleic acid had similar effects on oxalate absorption but was less effective than ricinoleic acid. Octanoic acid, a medium chain fatty acid, did not alter oxalate absorption of oxalate by a nonspecific alteration of mucosal permeability. These observations may further explain many of the clinical phenomena associated with enteric hyperoxaluria.
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PMID:Effect of bile salts and fatty acids on the colonic absorption of oxalate. 126 69

By using an ethylene glycol-induced urolithiasis model, we assessed the role of testosterone in the pathogenesis of urolithiasis. The intact and castrated male and female rats were fed with 0.5% ethylene glycol in drinking water for four weeks. The renal excretions of oxalate, citrate and other electrolytes were measured, and the stone and crystal deposit were examined microscopically. The results showed that drinking a loading of 0.5% ethylene glycol for four weeks produced hyperoxaluria in all rats, but the intact male rats excreted more urinary oxalate than any other groups of rats. The ethylene glycol-fed rats exhibited hypocitraturia except the castrated male rats. However, urolithiasis occurred in intact male but not female rats. Castration in male rats fed with ethylene glycol dramatically decreased the incidence of renal stone from 71.4% (5/7) to 14.3% (1/7). On the other hand, there was still no renal stone formed in the oophorectomized female rats which received ethylene glycol treatment. These data indicate that serum testosterone level plays a determinant role in urolithiasis formation.
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PMID:Determinant role of testosterone in the pathogenesis of urolithiasis in rats. 155 10

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.
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PMID:[The effects of high-dose ascorbic acid administration on the factors of lithogenesis in the rat]. 166 24

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.
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PMID:[Is sucrose a risk factor in calculus formation?]. 174 29

The influence of a calcium-rich mineral water on urine crystallisation in patients with recurring kidney stones was investigated. A calcium and magnesium rich water like the one tested increases the calcium and magnesium content of the urine but decreases oxaluria even after a dietary oxalate load.
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PMID:[Prevention of the recurrence of urinary lithiasis: mineral waters with high or low calcium content?]. 343 28

This study is presented as a debate on nephrolithiasis by a urologist and an internist. The reason is that in 1986 the urologist has become successful at desintegrating almost any stone without open surgery, whereas the internist's approach to the same problem is entirely based upon an understanding of pathophysiological mechanisms. After having reviewed the major risk factors for renal stone disease, i.e. small urine volume, hypercalciuria, hyperoxaluria, hyperuricosuria, very high or very low urine pH and hypocitraturia, the author shows that now it is not only possible to selectively correct each of these disorders, but that in doing so the internist does change the natural history of the disease. For instance, definite remissions have been obtained by advising patients to increase water intake, by administering thiazides to hypercalciurics, pyridoxine to some hyperoxalurics, allopurinol to hyperuricosurics, urease inhibitors to struvite stone formers and citrate to hypocitraturics. Therefore, the author concludes that the role of the urologist and that of the internist are complementary: although the former now desintegrates the stone without open surgery, the latter, who takes care of the same patient next, is now largely able to prevent relapse of nephrolithiasis after determining the cause of the disease.
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PMID:[Renal lithiasis: the internist's viewpoint 1986]. 373 61

As calcium oxalate stones are the most important component in urolithiasis, an experimental model has to be designed to clarify the pathogenesis and aid in their prevention. Hyperoxaluria as well as hypercalciuria were produced in rats by administering ethylene glycol (0.5%, in drinking water administered ad libitum) and 1-alpha (OH) D3 (0.5 micrograms/rat given every other day), respectively, for three to four weeks. Neither drug alone produced stones efficiently as did the combination regimen of these two compounds. The occurrence of stones was 77.3%, and with only a moderate degree of renal functional impairment. Biochemical and histological data were obtained using this model.
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PMID:[Experimental and clinical studies on calcium urolithiasis: (I) Animal model for calcium oxalate urolithiasis using ethylene glycol and 1-alpha (OH) D3]. 403 34

The preventive affects on recurrent renal calcium stones of water diuresis alone or combined with drugs aimed at lowering urinary calcium were evaluated prospectively in 51 patients with calcium nephrolithiasis. Following clinical and metabolic examination, the patients were allocated at random to 3 treatment groups: water diuresis alone (group I, n = 19) or associated with hydrochlorothiazide 50 mg/day (group II, n = 19) or with a neutral phosphate preparation 1500 mg/day (group III, n = 13). Results were assessed on the number of recurrences; 24-h urinary calcium was measured at regular intervals. The mean follow-up (2 years; range 1-4 years) was the same in all 3 groups. A significant fall in recurrence rate as compared with pre-treatment values was observed in groups I and II. The recurrence rate was the same in both groups during treatment. However, less patients had recurrences in group I (1/19) than in group II (5/19). No significant fall in recurrence rate was observed in group III, owing to some patients in this group having frequent recurrences. The recurrence rate was unrelated to clinical findings and biochemical values ( oxaluria , calciuria) measured before treatment and to the urinary Ca/Cr ratio calculated during treatment. This study confirms that water diuresis is effective in preventing recurrent renal calcium stones and that diuretics of the thiazide group reduce the number of patients with recurrences.
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PMID:[Incidence of lithiasic recurrence after a diuretic therapy, alone or combined with treatment by a thiazide diuretic or phosphorus]. 623 83

A shortened small intestine may end at a stoma or be anastomosed to the colon. Patients with a jejunostomy, but not those with a colon, lose large amounts of sodium. The intake and absorption of sodium can be increased by sipping a sodium-glucose solution; stomal loss can be reduced by restricting water or low-sodium drinks. If a stoma is situated less than 100 cm along the jejunum, a constant negative sodium balance may necessitate parenteral saline supplements. Gastric anti-secretory drugs or a somatostatin analogue reduce jejunostomy losses in such patients but do not restore a positive sodium balance. Loperamide or codeine phosphate benefit some patients. Magnesium deficiency can usually be corrected by oral magnesium oxide supplements. An elemental or hydrolysed diet is not beneficial. Patients with a jejunostomy can maintain a normal diet without fat reduction. When the colon is present, unabsorbed carbohydrate is fermented to absorbable short chain fatty acids. Unabsorbed long chain fatty acids and bile salts cause watery diarrhoea and increased colonic oxalate absorption with hyperoxaluria. Such patients benefit from a high carbohydrate, low-fat and low-oxalate diet. Parenteral nutrition is needed only by the few patients unable to maintain health or avoid socially disabling diarrhoea despite these measures.
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PMID:Review article: practical management of the short bowel. 769 44


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