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

In 6 male subjects the diurnal variation of urinary oxalic acid excretion was studied after ingestion of chocolate, a food stuff rich in oxalic acid. The ingestion of chocolate caused a striking but transient increase in urinary oxalic acid excretion due to its absorption in the upper gastrointestinal tract. The peak excretion rates occurred 2-4 h after the intake of the chocolate. The peak values were 235% of the fasting excretion rate in the trial with 50 g chocolate and 289% in the trial with 100 g chocolate and reached the amounts found in cases with primary hyperoxaluria. The administration of ranitidine had no influence on oxalic acid absorption. The transient hyperoxaluria observed seems to be an important factor for the formation of calcium oxalate calculi in patients on risk for stone disorders.
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PMID:Transient hyperoxaluria after ingestion of chocolate as a high risk factor for calcium oxalate calculi. 291 54

An assay system for the measurement of the rate of Calcium Oxalate Monohydrate (COM) seed crystal growth in a metastable solution of calcium chloride and sodium oxalate containing traces of 14C-oxalic acid was used to assess the inhibitory activity of pyrophosphate (10(-5) M-10(-4) M), citrate (10(-4) M-10(-3) M) and urines of normal and pyridoxine deficient rats. Both pyrophosphate and citrate were strong inhibitors of COM crystal growth and caused a 50% decrease in crystal growth rate at 1.50 X 10(-5) M and 2.85 X 10(-4) M respectively. Normal rat urine strongly inhibited the COM crystal growth, while pyridoxine deficient animals showed a significant (p less than 0.01) decrease in mean inhibitory activity as compared to pair-fed controls. A lowered urinary inhibitory potential accompanied with hyperoxaluria and hypercalciuria, which is known to be associated with pyridoxine deficiency, may be a contributory risk of calcium oxalate crystallization and stone formation.
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PMID:Inhibition of calcium oxalate monohydrate (COM) crystal growth by pyrophosphate, citrate and rat urine. 302 39

The increased oxalic acid absorption is a well documented finding in gastroenterological diseases. The malabsorption of bile acids and fat is important in the pathogenesis of the hyperoxaluria. The enteric absorption of 14C-labelled oxalic acid was measured in 49 patients with different diseases. The dihydroxy-trihydroxy-ratio of bile acids is significantly decreased in patients with hyperoxaluria over 20% of the ingested dosage. We didn't find any correlation between the excretion of oxalic acid and the intraduodenal pancreatic lipase activity.
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PMID:[Pancreatico-biliary secretion in enteral hyperoxaluria]. 325 36

Hyperoxaluria and calcium oxalate lithiasis have a multifactorial genesis in bowel diseases. The augmented synthesis of oxalic acid in the liver is of minor importance. A diminished bacterial degradation is to asses up to day only hardly. The increasing absorption is of highest importance by deficient production of calcium oxalate in the intestinal tract and by increasing permeability of colonic mucosa above all in steatorrhoea or in patients with augmented calcium absorption. The crystallization of calcium oxalate in the urine is promoted by shortage of vitamin A, citrate, zinc or magnesium.
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PMID:[Pathogenesis of hyperoxalurias and calcium oxalate calculi in intestinal diseases]. 331 5

Previous studies have provided evidence that an anaerobic bacterium, which degrades dietary oxalate to CO2 and formate, is present in colonic contents of a number of herbivorous species, laboratory rodents and humans. The present study examines the possibility that these bacteria degrade significant amounts of oxalate and can influence colonic oxalate absorption. Guinea pigs adapted to a diet containing 2% sodium oxalate or fed a normal diet were challenged with 67, 135, 170 or 200 mg of sodium oxalate containing 0.5 microCi of [14C]oxalate, which was injected into the cecum. Adapted animals excreted approximately 2% of the 14C in the urine, regardless of the dose, whereas unadapted animals excreted significantly higher amounts in the urine at the two lower doses and died at the two higher doses. Conversely, antibiotic treatment of adapted guinea pigs reduced the ability of their cecal flora to degrade oxalate, and a correspondingly greater percentage of an injected oxalate load was excreted in the urine. Oxalate degradation rates in cecal fluid were depressed by the secondary bile salt deoxycholate, and in vitro studies with pure isolates of guinea pig and human strains of oxalate degraders confirmed that these bacteria were highly sensitive to low concentrations of deoxycholate. Results indicate that these bacteria may be important in preventing excess absorption of oxalate and raise the possibility that the hyperoxaluria associated with bile salt malabsorption of ileal disease in part may be due to suppression of these bacteria by the bile salts.
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PMID:Intestinal oxalate-degrading bacteria reduce oxalate absorption and toxicity in guinea pigs. 337 43

The urinary excretion levels of oxalic acid, calcium, kynurenic, and xanthurenic acids and serum pyridoxal and pyridoxal phosphate concentrations were determined for nonbilharzial and bilharzial hyperoxaluric patients with or without urinary stones. The effects of pyridoxine and allopurinol treatment were also studied. The different groups studied showed elevated levels of urinary oxalic acid, calcium, kynurenic, and xanthurenic acids as well as decreases in serum pyridoxal and pyridoxal phosphate concentrations. These data indicate that nonbilharzial hyperoxaluric patients suffer from dietary B6 deficiency, whereas bilharzial hyperoxaluric patients may suffer from impaired pyridoxine phosphokinase activity. Pyridoxine supplementation is recommended for the treatment of nonbilharzial hyperoxaluric patients. Allopurinol may be the proper drug in the treatment of oxaluria and stone formation or of bilharzial patients.
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PMID:Biochemical studies on bilharzial and nonbilharzial hyperoxaluria: effect of pyridoxine and allopurinol treatment. 366 92

In order to find out whether hyperoxaluria can be demonstrated in patients on chronic (twice a week) haemodialysis, a group of 13 patients was investigated. These included one patient with proven primary hyperoxaluria, one suspected of having this disease and 11 patients in whom no information was available as to their oxalate metabolism. Oxalate concentrations in haemodialysate fractions and blood samples, taken before and after dialysis, were determined. The patient with primary hyperoxaluria had a plasma oxalate concentration before dialysis above 100 mumol/l and after dialysis above 25 mumol/l, while the oxalate concentration in haemodialysate at the start of dialysis was above 25 mumol/l and at the end above 10 mumol/l. The patient suspected of hyperoxaluria had similar values. Of the remaining 11 patients, one was shown to exhibit a transient hyperoxaluria, but the others showed a normal oxalate metabolism. A plasma oxalate/creatinine concentration ratio exceeding 0.1, and the calculated total quantity of oxalate removed by dialysis exceeding 2 mmol, also enabled a diagnosis of hyperoxaluria to be made. Hyperoxaluria can still be demonstrated in patients, who because of renal failure are subjected to haemodialysis. Measurements of oxalate in haemodialysate and plasma are valuable in cases where kidney transplantations are considered, especially when the particular patient exhibits hyperoxaluria.
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PMID:The determination of oxalate in haemodialysate and plasma: a means to detect and study 'hyperoxaluria' in haemodialysed patients. 370 74

Increased oxalic acid absorption, hyperoxaluria and oxalatelithiasis are found in many gastroenterological diseases. All persons receive 370 kBq 14C-oxalic acid for the measurement of oxalic acid absorption. The absorbed and in the urine excreted 14C-activities are measured with a scintillation spectrophotometer and scintillator composed of 2,5-diphenyloxazole(POP), 1,4-bis-(4-methyl-5-phenyl-2-oxazolyl)benzene (dimethyl-POPOP), naphthalene, toluene and ethyleneglycol monomethylether. Normal values of oxalic acid absorption are means +/- S = 7.17 +/- 1.87%/24 h (n = 40).
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PMID:[A method for measuring oxalic acid absorption]. 383 42

Accumulation of oxalate leads to hyperoxaluria and calcium oxalate nephrolithiasis in man. Since oxalate is a metabolic end product in mammals, the feasibility of its enzymic degradation has been tested in vivo in rats by administering exogenous oxalate oxidase. Oxalate oxidase, isolated from banana fruit peels, in its native form was found to be non-active at the physiological pH of the recipient animal. However, its functional viability in the recipient animal was ensured by its prior binding with ethylenemaleic anhydride, thus shifting its pH activity curve towards the alkaline range. Rats implanted with dialysis membrane capsules containing such immobilized oxalate oxidase in their peritoneal cavities effectively metabolized intraperitoneally injected [14C]oxalate as well as its precursor [14C]glyoxalate. The implantation of capsules containing coentrapped multienzyme preparations of oxalate oxidase, catalase and peroxidase led to a further degradation of administered [14C]oxalate in rats.
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PMID:Degradation of oxalate in rats implanted with immobilized oxalate oxidase. 394 4

Anaerobic bacteria that metabolize oxalic acid have only recently been isolated from the rumen and from other gastrointestinal habitats. They constitute a new genus and species, Oxalobacter formigenes. This report presents the first comparison of cultural counts of these organisms from human feces and indicates that numbers as high as 10(7)/g may be present in feces from normal humans. Rates of oxalate degradation by mixed bacterial populations in feces from seven normal humans ranged from 0.1 to 4.8 mumol/(g X h). With fecal samples from eight patients that had undergone jejunoileal bypass surgery, rates were much lower [0-0.006 mumol/(g X h)]. We propose that oxalic acid degradation by Oxalobacter formigenes may influence absorption of oxalate from the intestine and that lower rates or lack of oxalate degradation in the colons of jejunoileal bypass patients may contribute to the increased absorption of dietary oxalate and the hyperoxaluria commonly associated with such patients.
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PMID:Oxalate degradation by gastrointestinal bacteria from humans. 395 Jul 72


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