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

The urinary excretion of oxalate, calcium, citrate, magnesium, urate and creatinine and the inhibition of calcium oxalate crystal growth were determined in 30 patients operated with three different types of jejunoileal bypass. In addition the ion-activity products of calcium oxalate and calcium oxalate saturation were calculated. 15 of the patients had formed urolithiasis postoperatively. The patients were investigated on an out-patient basis with their ordinary diet. All patients had hyperoxaluria. The oxalate excretion did not seem to decrease with time after operation. The patients operated with a biliointestinal shunt had a significantly higher excretion of oxalate than those with the other two types of operation, indicating that variations in the anatomy of the small intestine after jejunoileal bypass might result in different absorption of oxalate or oxalate precursors. Urinary oxalate, calcium oxalate saturation and ion-activity products were higher whereas the excretion of calcium, magnesium and citrate was lower in patients than in controls. The urine volumes, excretion of creatinine and urate and inhibition of calcium oxalate crystal growth were equal in patients and controls. Analogous urine composition was found in patients both with and without urolithiasis with the exception of a higher magnesium excretion observed in stone formers.
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PMID:Urine composition following jejunoileal bypass. 682 41

We have previously shown that an oral glucose load increased both calciuria and oxaluria while the ingestion of fructose induced a rise in calciuria and a decrease in oxaluria. This latter effect remains unclear and might be linked to the reduced intestinal oxalate absorption subsequent to digestive intolerance in some subjects. Such a hypothesis could be enlightened by the study of a parenteral fructose load. Therefore in 7 healthy subjects, we compared the effects of fructose infusion (F) (15 min iv infusion at 0.185 mmol/kg BW/min) to a control glucose infusion (G) on urinary calcium and oxalate. In this study, glycemia and insulinemia increased less after (F) than after (G) (respectively + 21% vs + 216%, p < 0.001 and + 230% vs + 402%, p < 0.05) and phosphatemia decreased less after (F) than after (G) (-7% vs -14%, p < 0.05). Urinary calcium and oxalate increased only after (F) (respectively + 64%, p < 0.01 and + 60%, p < 0.05). Urinary uric acid, another urolithiasis factor, increased after both (F) and (G) (respectively + 45%; p < 0.01 and + 42%; p < 0.01) but uricemia increased only after (F) (+ 25%; p < 0.01). Our results suggest an additional reason to avoid the use of fructose in parenteral nutrition, particularly in individuals with a known history of either calcium oxalate or urate urolithiasis.
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PMID:Increase in urinary calcium and oxalate after fructose infusion. 760 7

Chocolate, a foodstuff rich in sucrose, fat and oxalate, is considered unsuitable in cases of obesity, diabetes mellitus, urolithiasis and postprandial hypoglycemia. However the pathophysiological effects of chocolate are poorly documented. Therefore we investigated the effects of ingestion of 100 g dark chocolate bar (45 g cocoa and 55 g sucrose) on carbohydrate, calcium and oxalate metabolisms in 10 healthy subjects. Results were compared to those of 55 g sucrose intake (control group) performed on another day. Chocolate caused i) a lesser but longer increase in plasma glucose, insulin, and C-peptide than sucrose (respectively +23% of baseline vs +60%, p < 0.001; +436% of baseline vs +755%, p < 0.01 and +200% of baseline vs +331%, p < 0.01), ii) a striking increase in triglyceridemia, calciuria and oxaluria (respectively +96%, p < 0.01; +147%, p < 0.01 and +213%, p < 0.001). Thus, chocolate (cocoa+sucrose) causes a lesser pancreatic stimulation than sucrose. However, the increases in both calciuria and oxaluria (induced respectively by sucrose and cocoa) following chocolate ingestion might contribute to urinary conditions favoring the development of calcium oxalate calculi.
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PMID:Increase in calciuria and oxaluria after a single chocolate bar load. 780 35

The serum and 24 hour urinary excretion levels of various lithogenic and inhibitory substances were assessed in 24 male patients with calcium stone and no previous history of urolithiasis and in 19 age-matched controls. Two groups did not differ significantly (P < 0.01) except in the excretions of sodium, citric acid (being higher in normals) and inorganic phosphate (being higher in patients). Fifty percent patients had hyperphosphaturia, 29.2% hypocitraturia, 20.8% hyperoxaluria and 16.7% hypercalciuria. The present data suggests that hypocitraturia in association with phosphaturia might be one of the main risk factors responsible for calcium urolithiasis in this area.
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PMID:Is hypocitraturia associated with phosphaturia--a potential cause of calcium urolithiasis in first-time stone formers. 799 62

Two patients with atypical manifestations of aberrant peroxisomal biogenesis are described. Contrary to previous studies, which had shown that Zellweger syndrome patients usually have normal levels of urinary oxalate excretion, the patients in the present study had evidence of abnormal oxalate metabolism in the form of hyperoxaluria and, in one of the patients, calcium oxalate urolithiasis. Activity of the liver-specific peroxisomal enzyme alanine:-glyoxylate aminotransferase (AGT), which is a major determinant of the level of endogenous oxalate synthesis in humans, was normal in one patient and markedly supranormal in the other. Using the technique of post-embedding protein A-colloidal gold immunoelectron microscopy, AGT was found to be mainly cytosolic in the livers of both patients, with significant amounts also localized in the nuclei. In a small minority of the hepatocytes of one patient, who was homozygous for the more common (major) AGT allele, large numbers of unidentified fibrillar arrays were found in the cytosol, which labelled heavily for immunoreactive AGT. The background cytosolic AGT labelling was markedly reduced in such cells when compared to the majority of cells that did not contain fibrils. In the other patient, who was heterozygous for the major and minor AGT alleles, there appeared to be low levels of mitochondrial AGT labelling. In the light of these data, the possible metabolic function of cytosolic AGT in the livers of panperoxisomal disease patients is discussed.
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PMID:Cytosolic compartmentalization of hepatic alanine:glyoxylate aminotransferase in patients with aberrant peroxisomal biogenesis and its effect on oxalate metabolism. 805 36

In order to better understand the role of diet in etiology of urolithiasis, 84 oxalo-phospho-calcic-lithiasic patients (52 men, 32 women) have been studied by a nutritional week-interview and by urinary and blood testing. Diet data were compared to an ideal standard. Total caloric intake was 2428 +/- 651 calories/d; this intake is high in 7% women and 40% men. 79% out of patients are fat. Protidic intake is 87 +/- 21 g/d higher than 1 g/kg/d in 84.5% of patients. Lipids are high in 38.9 +/- 7%, glucid are low in 45.3 +/- 7%. Calcium intake is 934 +/- 406 mg/d, sodium intake is 12.9 + 3 g/d. Water intake is 2305 +/- 759 ml/d. Different groups of patients are studied: a) 21 patients with mean age of 43 +/- 12 years have recurrent lithiasis (R). This group is compared to 48 patients with 37 +/- 44 years who have a single lithiasis. Half of (R) patients have hypercalciuria, hyperphosphaturia and hyperoxaluria. Diet study is no different between these two groups. b) Other groups are studied: 21 have hyperophosphaturia (HPU) without hypophosphoremia and they have hypercalciuria, hyperuraturia and high urinary urea; diet shows higher glucicid and potassium intake than group with normal phosphaturia; 23 have hypercalciuria (HCU) and high uraturia and phosphaturia: diet study shows no difference with a group with normal calciuria. 21 have hyperoxaluria (HOU): diet study of a normal oxaluric group shows higher lipid intake, lower glucidic and calcium intake; 22 have hyperuraturia (HAU) and higher urinary urea, sodium and potassium than normouraturia group: in this group potassium intake is higher.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Results of dietary evaluation during calcium oxalate and calcium phosphate lithiasis]. 814 88

Evidence for the suitability of spot urines for selective screening in children was obtained by comparing the 24-hour urinary oxalate excretion with the ratio of urinary oxalate to creatinine [mmol/mol] in spontaneously voided urine samples. Spot urines of 169 healthy children aged 1 day to 13 years were analysed in order to establish reference values for the urinary oxalate/creatinine ratio in relation to age and body surface area. Oxalate was measured by automated ion chromatography. Results showed an inverse relationship between the oxalate/creatinine ratio and age. The highest ratios, 131 +/- 57 mmol/mol (mean +/- 2 SD), were found in infants. At age two years, the ratio was 84 +/- 55, at age five years 56 +/- 35, and for children older than ten years 42 +/- 31. This finding can be explained by the gain of muscle mass and hence increased creatinine production with increasing age. Data for the urinary oxalate/creatinine ratio are presented according to body surface area for the assessment of children with abnormal growth. In 19 urine samples from nine patients with primary hyperoxaluria, the oxalate/creatinine ratio greatly exceeded (286-2022 mmol/mol) the above reference ranges. We therefore propose the determination of the oxalate/creatinine ratio in spot urines for the selective screening for hyperoxaluria in children with nephrocalcinosis or urolithiasis.
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PMID:Determination of oxalate excretion in spot urines of healthy children by ion chromatography. 816 90

The hypothesis that mild hyperoxaluria is more important than hypercalciuria in the pathogenesis of urolithiasis is re-examined in the light of new evidence. Small increments in urinary oxalate in the normal to high-normal range are much more critical than similar rises in urinary calcium for increasing the relative supersaturation of urine with respect to calcium oxalate, the oxalate/calcium ratio in urine, the total volume of calcium oxalate crystals excreted, the proportion of abnormally large crystals and aggregates of calcium oxalate and the severity of the disorder as defined by the recurrence rate of stone-formation. Data from the Arabian Peninsula, where the prevalence of calcium-containing stones is considerably higher than in the West, have shown that this occurs in spite of the almost complete absence of hypercalciuria. On the other hand, there is a strong association between stone-formation and the occurrence of mild hyperoxaluria. The life-time expectancy of stone-formation in men from various countries is strongly correlated with the average daily excretion of oxalate in the urine of the normal men in these countries. This relationship extends to include patients with enteric and hereditary hyperoxaluria. There is no such relationship, however, between the life-time expectancy of stones and urinary calcium excretion in the same populations. Studies on the regulation of urinary oxalate indicate that it is largely controlled by the quantity of "free" dietary oxalate available for absorption in the lower intestine. This can be calculated from the intakes of calcium and oxalate and the urinary excretion of calcium.
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PMID:Importance of mild hyperoxaluria in the pathogenesis of urolithiasis--new evidence from studies in the Arabian peninsula. 831 8

Urolithiasis in pediatric patients has been perceived as uncommon, and the appropriate evaluation and management have been controversial. To determine the clinical characteristics, types of stone problems, and outcomes of pediatric patients with urolithiasis encountered in a referral center, we retrospectively assessed 221 patients (113 girls and 108 boys) with urolithiasis examined at the Mayo Clinic between 1965 and 1987. The median age at onset of symptoms was 11 6/12 years among the female patients and 10 6/12 years among the male patients. Analysis of stone constituents in 122 patients showed the proportion of calcium oxalate (44.7%), calcium phosphate (23.6%), and cystine (8.1%) stones to be similar in all age-groups. Overall, struvite stones were found in 17.1% and uric acid stones in 1.6% of patients. Conditions that predisposed to metabolic urolithiasis were identified in 115 patients (52%). Hypercalciuria was confirmed in 49 of 145 patients (33.8%) and hyperoxaluria in 25 of 124 (20.2%). Eight of 96 patients had hyperuricosuria, and 5 of 54 had hypocitraturia. Forty-one patients (18.6%) had infection-related stones. Of 66 patients with structural anomalies of the genitourinary tract, 24 (36%) had metabolic abnormalities and 26 (39%) had chronic infection. Among patients with chronic infection, 29% had metabolic abnormalities. Of the 221 patients, 148 (67%) had two or more stones during a mean follow-up of 59 months. Among 140 patients with 12 months or more of follow-up, metabolic activity was present in 31 (22.1%) at the time of most recent examination. Overall, 166 of 221 children (75.1%) were found to have factors that predisposed to urolithiasis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Urolithiasis in pediatric patients. 847 76

Primary hyperoxaluria type I (PHI) is a cause of end-stage renal disease in young people. It is caused by deficient activity of hepatic peroxisomal alanine:glyoxylate aminotransferase (AGT), which results in hyperoxalemia and hyperoxaluria. The consequent urolithiasis and nephrocalcinosis result in renal impairment, with further reduction in oxalate excretion and eventual systemic oxalosis. Historically, renal transplantation has yielded very poor results in these patients because of recurrent oxalosis of the graft. Within the last 10 years, combined hepatorenal transplantation has been successfully applied, simultaneously correcting the metabolic lesion in the liver and replacing the damaged kidneys. It has, however, become apparent that medical therapy with vigorous hydration, inhibitors of stone formation and pyridoxine (AGT co-factor), may be successful at delaying, and occasionally in preventing, urolithiasis in some hyperoxaluric patients, particularly those whose hyperoxaluria is reduced by pyridoxine. This, together with intensive perioperative management and modern surgical methods of stone management such as lithotripsy, laser or ultrasound stone fragmentation, and percutaneous nephrolithotomy, means that renal transplantation alone may be feasible in selected patients. We describe a patient with PHI with clinical and biochemical evidence of significant residual AGT activity who underwent a successful live-related renal transplantation with excellent renal function and no stone recurrence 1 year posttransplantation. The appropriate transplantation strategies for these complex patients are discussed and include isolated renal transplantation for those patients who are without significant systemic oxalosis and have evidence of residual AGT activity.
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PMID:Selective renal transplantation in primary hyperoxaluria type 1. 865 Dec 56


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