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

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

Piridoxilate (P) is given in cases of angina pectoris or arteritis. It is an intramolecular association of glyoxylic hemiacetal salts of pyridoxine. Glyoxylate has a membranous protective action; pyridoxine is used for the theoretical purpose of preventing oxidation of glyoxylic acid to oxalic acid. We have observed 12 patients with an active calcium oxalate lithiasis who had been taking P for many years. Hyperoxaluria was present in all patients and decreased significantly when the drug was interrupted. Significant hyperoxaluria was also observed in volunteers after ingestion of P (600 mg per day) or i.v. (200 mg). We have obtained experimental calcium oxalate urinary stones after intraperitoneal injection of P to Wistar rats. Piridoxilate represents an important lithogenic factor.
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PMID:[Iatrogenic oxalic lithiasis caused by pyridoxilate]. 409 36

The normal value of oxaluria, as determined by gasliquid chromatography, is about 30 mg/24 h. In most cases of renal stone formation (60-70%) the stones are composed of calcium oxalate alone or associated with calcium phosphate. The more evolutive the disease, the higher the oxaluria. The part played by oxaluria in renal stone formation and the need to include its determination in regular examinations of stone formers must be stressed. Treatment of hyperoxaluria is both medicinal and dietetic : control of oxalic acid-rich food intake and reduction of the intestinal absorption of oxalate caused by calcium-deprived diets. The diet must be completed by therapeutic measures aimed at reducing the oxaluria and increasing the urinary factors preventing crystallization.
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PMID:[Oxaluria in urinary lithiasis]. 622 3

Calcium and oxalate were studied in daily, fasting and postprandial urine specimens from healthy subjects and patients with idiopathic renal calcium stones in response to a test meal free of oxalate, and supplemented with calcium and 14carbon-oxalic acid. The data showed that the amount of oxalate in fasting urine of patients with stones did not differ from that in controls. Generally, patients with stones had considerable postprandial hyperoxaluria in terms of excretion and concentration, associated with a significantly higher degree of supersaturation with regard to calcium oxalate compared to controls. These findings were paralleled by decreased intestinal absorption of 14carbon-oxalate and by unchanged 24-hour urinary oxalate. Although the source of increased postprandial oxalate in patients with stones is not clear the possibility of enhanced de novo synthesis from oxalate precursors is discussed. In patients with different types of calciuria the 2 main risk factors (hyperoxaluria and hypercalciuria) for the process of stone formation are recognizable more readily in the postprandial urine specimens than in fasting or daily urine specimens.
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PMID:Postprandial hyperoxaluria and intestinal oxalate absorption in idiopathic renal stone disease. 647 Dec 6

Because of mounting evidence of precipitation of calcium oxalate in the soft tissues of patients with end-stage renal disease (ESRD) on maintenance hemodialysis, the plasma oxalate concentrations and calculated dialysis removal of oxalate were studied in seven patients without evidence of either primary or absorption hyperoxaluria prior to ESRD. A reversed-phase high-pressure liquid chromatographic method was developed to quantitate serum oxalate. Mean value +/- SE in four healthy controls was 28 +/- 5 mumol/L, and in the seven patients it was 187 +/- 15 mumol/L predialysis and 89 +/- 11 mumol/L postdialysis. Oxalate deposition in the soft tissues of ESRD patients is the consequence of sustained hyperoxalemia. Oxalate removal by dialysis was calculated from the four-hour oxalate clearance. Since the ionic radii of phosphate and oxalate are similar, total oxalate clearance was calculated midpoint of dialysis. Mean oxalate removal/dialysis was 3.01 +/- 0.283 mmol. On a daily basis this value was 1.645 +/- 0.155 mmol, which is about threefold the normal oxalate excretion rate. It is not significantly different from the excretion rate in absorption oxalurias but is less than that in primary hyperoxaluria. Therefore, it is concluded that hyperoxalemia in ESRD results from loss of renal excretion, failure of hemodialysis to remove enough oxalate to maintain a normal serum concentration, and increased intestinal absorption of oxalate and/or increased endogenous production.
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PMID:Oxalate removal by hemodialysis in end-stage renal disease. 647 42

The authors report on metabolic studies on growing domestic pigs with resected ilea on a diet supplemented with oxalic acid and calcium. The content of calcium, magnesium and phosphate in the kidneys and ribs was determined and their excretion in urine was measured. The supplement of oxalic acid in the diet mainly affects the calcium content of the kidneys. It is also likely that oxalic acid inhibits the accumulation of calcium in the skeleton. Hyperoxaluria and hyperphosphaturia were established, whereas significantly less calcium and magnesium were excreted. The results of these animal experiments confirm previous clinical findings.
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PMID:[Clinical and animal experiment studies on the pathogenetic significance of small intestine diseases and resections for urolithiasis]. 663 70

The circadian (circannual for oxalic acid) variations of 13 urinary variables (volume, creatinine, calcium, oxalic acid, glycolic acid, 17-ketosteroids, 17-hydroxycorticosteroids, phosphates, urea, uric acid, chloride, sodium, and potassium) have been documented in 7 calcium oxalate renal stone formers and 7 healthy men (control group). Urine was collected every 4 h over a period of 24 h. All subjects had the same synchronization: diurnal activity from 07(00) to 23(00) +/- 1 h and nocturnal rest; meals were given at fixed clock hours (08(00), 12(30) and 20(00) +/- 1 h). A statistically-significant rhythm (p less than 0.05) was validated for all variables except urea and calcium in healthy men. In renal stone formers, 6 variables (calcium, oxalic acid, and glycolic acid in particular) had no detectable circadian rhythm. However, a periodicity of c. 8 h (ultradian rhythm) was demonstrated for calcium and oxalic acid with peaks being located around 02(00), 10(00), and 18(00). No circannual variations in oxalic acid output could be observed. The present study shows an alteration of the periodicity of calcium and oxalic metabolisms, i.e. the loss of a circadian (24-h) rhythm and the occurrence of an ultradian rhythm of 8 h. The risk of calcium-oxalate crystallisation appears thus greater at 02(00), 10(00), and 18(00). Furthermore, any study dealing with oxalic acid excretion should state the season of urine collection when comparing renal stone formers and healthy subjects, as significant differences in oxaluria may appear during the summer months and not during the rest of the year.
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PMID:Alterations in circadian rhythmicity in calcium oxalate renal stone formers. 686 98

1. Seventeen healthy controls and 63 patients with idiopathic calcium stone disease of the urinary tract were investigated for urinary calcium and oxalate excretion and for [14C]oxalate intestinal absorption. 2. Under comparable controlled dietary intake a significant increase in calcium excretion as found in patients with stone disease. Oxalate excretion and [14C]oxalate intestinal absorption were mildly but not significantly increased. When patients with stone disease were subdivided into normocalciuric and hypercalciuric subjects, oxalate excretion and [14C]oxalate absorption were significantly increased in the latter. There was a significant direct relationship between calcium excretion and both oxalate excretion and [14C]oxalate absorption. 3. [14C]Oxalate absorption increased significantly in 22 stone-formers when dietary calcium was changed from normal to low. 4. The kinetics of [14C]oxalate intestinal absorption showed that the main difference between normocalciuric and hypercalciuric subjects occurred within the first 6 h after the oxalate-labelled meal. 5. These results confirm that mild hyperoxaluria is a frequent feature of idiopathic calcium stone disease even when patients and controls are studied under controlled dietary conditions. Our data are consistent with the hypothesis that hyperoxaluria is secondary to calcium hyperabsorption and is upper intestinal in origin.
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PMID:Hyperoxaluria in idiopathic calcium stone disease: further evidence of intestinal hyperabsorption of oxalate. 710 33

A 32-year-old women was treated for overweight by gastrointestinal bypass surgery. Following surgery, repeated calcium oxalate nephrolithiasis was observed and secondary hyperoxaluria was diagnosed. Treatment with low oxalate and fat diet resulted in normal urinary oxalic acid excretion; no further stone formation was observed.
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PMID:[Nephrolithiasis after intestinal bypass: successful treatment with a low-fat diet]. 731 47

Clinical and biochemical data were obtained from 50 patients in whom stones form and 20 controls to set up and test a screening procedure for detecting metabolic abnormalities related to the formation of urinary calculi and to provide a preliminary estimate of the frequency of these disorders in our area. A comparison between patients in whom stones form and controls in terms of the quantitative biochemical parameters evaluated (serum calcium, uric acid and inorganic phosphate, and urine calcium, uric acid, inorganic phosphate, oxalic acid, xanthine and alpha-amino-nitrogen) showed a significant difference only with respect to excretion of urinary oxalate by adults, which was higher in patients in whom stones form. Metabolic disorders were detected in 15 adult patients with stones. Of these patients 9 had isolated hyperoxaluria, 3 had incomplete renal tubular acidosis, 1 had idiopathic hypercalciuria, 1 had heterozygous cystinuria and 1 had idiopathic hypercalciuria associated with heterozygous cystinuria. These results suggest a high frequency of metabolic abnormalities in patients in whom stones form in our area, so that the wider use of the screening used here may benefit a large number of patients with preventive and therapeutic measures.
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PMID:Metabolic factors in urolithiasis: a study in Brazil. 742 May 93


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