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

Enteric hyperoxaluria and oxalate urolithiasis in patients with ileal resection seem to be caused by intestinal hyperabsorption of oxalate. The mechanism responsible for hyperabsorption of oxalate is not known. Intestinal transport of oxalic acid was therefore examined by an in vitro technique in rat intestine. Oxalic acid was absorbed by a mechanism of simple passive diffusion. The rate of absorption decreased from the colon to the duodenum (colon greater than ileum greater than jejunum greater than duodenum). Bile acids enhanced oxalic acid absorption in the large and small intestine and increased extracellular space; calcium, however, markedly decreased mucosal-serosal transport of oxalic acid. Cholestyramine known to reduce oxalate excretion in hyperuxaluria associated with ileal resection did not directly affect absorption of oxalic acid, but decreased the enhanced absorption of oxalic acid induced by bile acids. The results suggest that the beneficial therapeutic effect of cholestyramine in hyperuxaluria is rather mediated by its bile acid binding activity than by direct binding of oxalic acid.
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PMID:Intestinal oxalate absorption. I. Absorption in vitro. 41 86

Excretion of oxalic acid in urine was measured in 28 healthy and 97 patients with gastrointestinal diseases. We found significantly higher values in the following groups: patients after resection of parts of the small intestine, patients with sprue and other diseases with malabsorption, patients with M. Crohn of the small intestine, colitis ulcerosa and granulomatosa, patients with chronical diseases of the pancreas gland and patients with cirrhosis of the liver. In 4 patients after resection of parts of the small intestine or pancreas urolithiasis could be verified. Reduction of fat and food without ballast reduced the excretion of oxalic acid in urine. Hyperoxaluria correlied significantly with the following parameters: excretion of fat in feces, exhalation of 14CO2 in the glykocholate breath test, resorption of vit. B12 and the length of resected small intestine. This form of hyperoxaluria is caused by hyperresorption of oxalic acid from food. The mechanism of this hyperresorption is not clarified yet, an important factor seems to be ill resorption of fat.
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PMID:[Hyperoxaluria in intestinal and liver diseases]. 83 13

Five patients with jejunoileal shunt for morbid obesity in whom postshunt hyperoxaluria and recurrent urinary tract calculi developed are presented. All the stones were composed of calcium oxalate. The twenty-four hour urinary oxalic acid levels were also elevated in twenty of twenty-six patients who had had jejunoileal shunt for six months or longer. No correlation was present between urolithiasis and the degree of hyperoxaluria.
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PMID:Hyperoxaluria and urinary tract calculi after jejunoileal bypass. 111 99

To better define the relative role of metabolic factors in the recurrence of stone formation, we studied the 24-hour urinary excretion of calcium (uCa), citrate (uCit), oxalic acid (uOx) and uric acid (uUa) in 73 male patients with primary calcium oxalate urolithiasis. According to the episodes of stone formation per year, we identified 51 recurrent stone formers (RSF) and 22 single stone formers (SSF). 20 normal adult males constituted the control group (C). uCa and uOx were higher in RSF than in C, but quite similar in SSF and RSF. The only difference between RSF and SSF was uCit, significantly lower (2.06 +/- 1.04 mmol/24 h) in RSF than in SSF (3.22 +/- 1.18 mmol/24 h, p less than 0.001) and in C (3.42 +/- 1.33 mmol/24 h, p less than 0.001). Hypocitraturia (uCit less than 1.5 mmol/24 h) was found in 16 of 51 RSF (31.4%) and in 1 of 22 SSF (4.5%). These data confirm that high levels of uCa and uOx represent a risk factor for lithogenesis, but also strongly indicate the low uCit excretion as the most important urinary abnormality accounting for the recurrence of calcium oxalate stones.
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PMID:Low urine citrate excretion as main risk factor for recurrent calcium oxalate nephrolithiasis in males. 152 45

Oxalic acid seems to play a far greater role in the formation of calcium oxalate stone than calcium. Three grams of calcium lactate and 3 g of sodium potassium citrate were administered to 46 urolithiasis patients, whose stones were mainly composed of calcium oxalate. Urinary oxalate level was reduced significantly without raising urinary calcium level by the administration of the two drugs for two weeks. The reduction of urinary oxalic acid was particularly remarkable in patients without hypercalciuria. The mechanism of action of these drugs was discussed.
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PMID:Reduction of urinary oxalate by combined calcium and citrate administration without increase in urinary calcium oxalate stone formers. 154 Oct 59

Because human urine contains various substances which can affect each other, it is quite difficult to clarify the mechanism of formation of calcium oxalate (CaOx) crystal in urine. The authors recently determined CaOx crystalline content and the concentrations of other substances in urine specimens from patients with urolithiasis and healthy volunteers, and subjected the data to multi-regressive analysis for the purpose of assessing the effect of these urinary substances on CaOx crystal formation. 1. In analysis of urine from patients with urolithiasis, the partial correlation coefficients of CaOx crystal formation with oxalic acid, sodium, calcium, uric acid magnesium were 0.67, 0.28, 0.18, and -0.10, respectively. The formula of regression was as follows: Amount of CaOx crystal (X 10(6) microns3/ml) = 3.59 X 10(-2) Ox (mM/L) + 4.72 X 10(-3) Ca (mM/L) + 4.52 X 10(-3) Na (mM/L) + 2.51 X 10(-4) UA (mM/L) -2.39 X 10(-2) Mg (mM/L) -1.65. The multiple correlation coefficient was 0.759. Thus, in patients with urolithiasis, urinary crystal formation was most dependent on the oxalic acid level, sodium, calcium, and uric acid were found to promote crystal formation, while magnesium to suppress it. 2. In analysis of urine from healthy volunteers, the partial correlation coefficients of CaOx crystal formation with oxalic acid and inorganic phosphorus were 0.51 and -0.24, respectively. The formula of regression was as follows: Amount of CaOx crystal (X 10(6) microns3/ml) = 1.91 X 10(-2) Ox (mM/L) -3.43 X 10(-4) P (mM/L) +0.29 The multiple correlation coefficient was 0.525.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Studies on calcium oxalate crystal formation in urolithiasis. Multi-regressive analysis of urinary CaOx crystalline volumes and the effects of urinary various substances on CaOx crystal formation]. 187 73

Oxalic acid seems to be more important for the formation of calcium oxalate stone than calcium. Three grams of calcium lactate and 3 g of uraly U were administered to 35 urolithiasis patients, whose stones were mainly composed of calcium oxalate. Urinary oxalate level was reduced significantly without raising urinary calcium level by the administration of the two drugs for two weeks. The reduction of oxalic acid was particularly remarkable in patients without hypercalciuria. The mechanism of action of these drugs and the relation to dietary management were discussed.
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PMID:[Reduction of urinary oxalate excretion by administration of calcium and citrate]. 260 Dec 15

In 13 patients suffering from recurrent calcium-oxalate urolithiasis the circadian course in the excretion of urinary components was investigated before and during treatment with a combination of allopurinol and benzbromarone. The patients were given a diet standardized in food and liquid intake. Urine was collected for 3 days every 3 h from the 7th day of standard diet. On days 8 and 9 each patient received one tablet of the combination. On all 3 days of urine collection a constant circadian course of urine volume was observed; pH values also showed a nearly identical course on all 3 days with increased daytime and low night values. Maximum excretion of uric acid under dietary conditions was discovered between 11 a.m. and 5 p.m. (day 7). After the first application of the compound (day 8, 8 a.m.) a transient increase in uric acid excretion was observed in the third collection period (2-5 p.m.), followed by a sharp decrease. Following the second application (day 9) the transient increase of the uric acid excretion was clearly diminished. Uric acid excretion in the 24-h urine also decreased steadily from 3.46 mmol/day (control) to 3.25 and 3.06 mmol/day (treatment). Serum uric acid decreased significantly from 324.5 to 275.6 mumol/l. After the first application of the compound (day 8) moderate changes of the urinary components - oxalic acid, Na, K, and chloride - significant changes of Ca were observed, whereas after the second application of the compound (day 9) the values no longer differed from control values.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Effect of an allopurinol/benzbromaron preparation on the composition of urine in a circadian course]. 357 81

It is well known that the urinary excretion of oxalic acid is one of the main determinants for urinary stone formation. From 1950 to 1978 a saturated oxalic acid solution was used in a repainting and cleaning process for railroad cars in Norwegian railroad workshops. With the use of a questionnaire, the cumulative prevalence of urolithiasis-induced colic episodes was registered in the Sundland railroad depot. Forty-two (11.9%) out of 353 male workers not exposed to oxalic acid reported having had one or more such stone colic episodes. The corresponding figure for 15 individuals who had a very high exposure to oxalic acid was 8 (53.3%). Also workers in other departments, occasionally exposed to oxalic acid, had an increased stone colic prevalence rate, a finding suggesting a positive dose-response relationship. There was an increased frequency of stone colic episodes in the age group 40-69 years. Seven heavily exposed workers in the paint shop reported initial pollakiuria and slight dysuria during the exposure. The study indicates a causal relation between urinary stone formation in the investigated railroad shopmen and their exposure to oxalic acid at work.
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PMID:Urolithiasis in railroad shopmen in relation to oxalic acid exposure at work. 400 3

Pyridoxilate is a salt formed from glyoxylic acid and pyridoxine. It has been used therapeutically as an antianoxic drug in the treatment of various arterial complaints. Its use is based theoretically on its ability to block the conversion of glyoxylic acid into oxalic acid. The following cases suggest, however, that pyridoxilate can cause stones. Intraperitoneal injection of glyoxylate in doses of 130 mg/kg will cause oxalate stones in rats. The same effect results from injection of 427 mg/kg pyridoxilate (i.e. an equivalent dose of glyoxylate). In human subjects, intravenous injection of 200 mg of pyridoxilate results in a fourfold increase in the urinary oxalic acid content in the two hours following the injection. Thirteen cases of chronic progressive oxalate stone disease have recently been reported in patients receiving a prolonged course of pyridoxilate at 450 to 600 mg daily. Eight of these patients had no previous history of lithiasis. Oxaluria levels of 80 to 100 mg daily are observed in all cases of lithiasis in patients receiving pyridoxilate. The levels fell after cessation of the pyridoxilate treatment, and reverted to normal (30 mg/24 hours) in all but three patients. These three patients maintained levels of close to 50 mg and all three had a previous history of urolithiasis.
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PMID:[Calcium oxalate stones and hyperoxaluria secondary to treatment with pyridoxilate]. 408 39


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