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

The incidence of urolithiasis was registered in 87 patients with chronic inflammatory bowel disease and compared with that of renal oxalate excretion. All patients were studied while on a standardized diet with fixed amounts of fat, calcium, and oxalate. Pyelography had been performed in all. Nine, or 35%, of 26 hyperoxaluric patients had urolithiasis, compared with 14, or 23%, of 61 patients were normal renal oxalate excretion, the difference being statistically insignificant. No significant difference in urinary oxalate or urinary calcium in stone-formers as compared with non-stone-formers could be demonstrated. Oxalate was a more frequent component of calculi in patients with normal renal oxalate excretion than in patients with hyperoxalura. Thus, we were unable to demonstrate an increased incidence of urolithiasis in patients with hyperoxaluria compared with a control group with normal renal oxalate excretion. Our results cast doubt on the concept that enteric hyperoxaluria per se is the cause of stone diathesis in chronic inflammatory bowel disease.
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PMID:Urolithiasis and hyperoxaluria in chronic inflammatory bowel disease. 48 60

The renal handling of oxalate was studied by the injection of 14C-oxalate together with inulin as a glomerular marker into the renal artery in 6 patients. From the recovered amounts of the injected substances in the urine, time-concentration curves were constructed. Oxalate was excreted into urine 2.31 +/- 0.05 (SE) fold when compared to inulin. The maximal concentration of oxalate occurred at the same time as inulin, and there was no urinary precession of oxalate in comparison to inulin. From this part of the study we conclude that oxalate in addition to its filtered amount can probably enter the early part of nephron. In a second type of study, plasma levels of oxalate and inulin were observed over a period of 180 min, following intravenous injections in 7 volunteers. The decline of oxalate plasma concentrations followed first-order kinetics. Calculation of the rate constants of elimination assuming the 'one compartment open' model resulted in an oxalate to inulin ratio of 1.21 +/- 0.05. The oxalate half-life of elimination was 92 +/- 8 min, whereas that of inulin amounted to 112 +/- 9 min. The higher value of the calculated volume of distribution of oxalate compared to that of inulin indicates that oxalate enters a larger space than the extracellular fluid volume. The urinary recovery of intravenously injected oxalate was 97.2 +/- 1.4%, indicating that oxalate is excreted exclusively by the kidney. The observed differences of oxalate excretion, obtained with these two methods, could be attributed to the higher amount of ionized oxalate in the disequilibrium technique (rapid injections), entering the urine in a higher rate. Such a mechanism could explain the hyperoxaluria in calcium oxalate stone-forming patients.
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PMID:Renal elimination kinetics and plasma half-life of oxalate in man. 49 45

Hydroxypyruvate and glycolate inhibited the oxidation of [U-14C]glyoxylate to [14C]oxalate in isolated perfused rat liver, but stimulated total oxalate and glycolate synthesis. [14C]Oxalate synthesis from [14C]glycine was similarly inhibited by hydroxypyruvate, but conversion of [14C1]glycolate to [14C]oxalate was increased three-fold. Pyruvate had no effect on the synthesis of [14C]-oxalate or total oxalate. The inhibition studies suggest that hydroxypyruvate is a precursor of glycolate and oxalate and that the conversion of glycolate to oxalate does not involve free glyoxylate as an intermediate. [14C35Hydroxypyruvate, but not [14C1]hydroxypyruvate, was oxidized to [14C]oxalate in isolated perfused rat liver. Isotope dilution studies indicate the major pathway involves the decarboxylation of hydroxypyruvate forming glycolaldehyde which is subsequently oxidized to oxalate via glycolate. The oxidation of serine which is subsequently oxidized to oxalate via glycolate. The oxidation of serine to oxalate appears to proceed predominantly via hydroxypyruvate rather than glycine or ethanolamine. The hyperoxaluria of L-glyceric aciduria, primary hyperoxaluria type II, is induced by the oxidation of the hydroxypyruvate, which accumulates because of the deficiency of D-glyceric dehydrogenase, to oxalate.
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PMID:The synthesis of oxylate from hydroxypyruvate by isolated perfused rat liver. The mechanism of hyperoxaluria in L-glyceric aciduria. 62 64

Oxalate-urolithiasis and hyperoxalaria have been reported to be a frequent complication in patients with small bowel disease, especially in patients with ileal resection due to Crohn's disease. Hyperabsorption of oxalate seems to be the main patholgenetic factor for "enteric" hyperoxalaria. Intestinal absorption and urinary excretion of oxalate was measured in patients with various gastrointestinal diseases after oral or rectal administration of 14C-oxalate. Kinetic data suggest that 14C-oxalate is absorbed in the small, the large bowel and the rectum as well. Oxalate absorption was decreased in patients with a colectomy and in active ulcerative colitis, but increased in patients with ileal resection, chronic liver disease, and steatorrhea due to chronic pancratitis or sprue. There existed a positive correlation between 14C-oxalate absorption and the amount of fecal fat excretion. The data suggest that hyperoxaluria and hyperabsorption of oxalate are not a specific finding in patients with bile acid malabsorption, but may occur too, in steatorrhea without alteration of bile acid metabolism.
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PMID:[Enteric hyperoxaluria. I. Intestinal oxalate absorption in gastrointestinal diseases (author's transl)]. 68 26

On the basis of to-day knowledge about metabolism and excretion of oxalic acid, the rationale of therapy of stone pathology is revieved. The problems of both primary and secondary oxaluria and of inhibiting factors of cristalisation are particolarly discussed.
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PMID:[Current trend in the medical treatment of oxalic calculosis]. 74 36

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

In the female rat intoxicated with ethylene glycol the oxaluria increases with the degree of intoxication. The increase is less in the animals treated with succinimide. The comparative study of the results of the dosages made with gas-liquid-chromatography and by various colorimetric methods show that this later gives varying results and underestimates high concentrations of oxalic acid. The result is that any study based on results of dosages of urinary oxalic acid made by colorimetry must be taken with some reserve, and this on whether the oxalic lithiasis is experimentally induced or human, or whether its evolution is spontaneous or influenced by a therapeutic.
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PMID:Effect of succinimide on hyperoxaluria in the rat estimated value of the different dosing methods of oxaluria. 88 49

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

A case of massive ingestion of ethylene glycol is described. The clinical characteristics of this disorder such as persistent metabolic acidosis and oxaluria as well as changes in serum osmolality that may accompany ingestion of certain toxins are emphasized. The rapid clearance of ethylene glycol from the blood during hemodialysis is noted and the use of ethyl alcohol to block metabolic conversion of ethylene glycol to oxalic acid, which is also a toxin, is described. The importance of early diagnosis and therapy is stressed.
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PMID:"Bicarbonate resistant" metabolic acidosis in association with ethylene glycol intoxication. 127 68

The effect of calcium concentration (0-10 mmol 1(-1)) on oxalate uptake and transport was investigated in vitro using everted gut segments and sacs. Increase in calcium concentration in the incubation medium led to an increase in the amounts of precipitated oxalate on the intestine; however, the net oxalate flux to the serosal side decreased. The ions, i.e. Ca2+, Ox2-, H2PO4-, HPO4(2-), present in the incubation medium favoured formation of hydroxyapatite and calcium oxalate crystals, as evidenced by Equil II analysis and free energy of the system. The nature of precipitates was confirmed by elemental analysis, X-ray diffraction spectrometry and electron microscopy. Oxalate precipitated on the intestine following incubation with calcium could be released into a calcium- and oxalate-free medium. Animals fed oxalate in the absence and presence of calcium revealed that, during 1 h in the absence of calcium, oxalate moved down the intestinal tract as a distinct peak of greater than 50% (70-90 cm in the intestine), leaving less than 10% in the stomach and first 50 cm of the intestine. In the case of animals fed calcium along with oxalate, 35% of the oxalate was still present in the stomach, and the amounts of oxalate in the intestinal segments gradually increased from 4.5% to 21.7% (0-90 cm) and dropped to 2.1% in the next 20 cm. Since oxalaemia and oxaluria appear to be influenced by intestinal oxalate absorption, the present observations may help to improve understanding of the pathophysiology of disorders exhibiting altered oxalate metabolism.
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PMID:Effect of calcium on oxalate uptake and transport by the rat intestine. 133 82


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