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

Pyridoxine in doses of 250-500 mg daily by mouth was administered to 12 patients suffering from recurrent calcium oxalate renal calculi and idiopathic hyperoxaluria. This therapy decreased urinary oxalate excretion significantly (p less than 0.025) during up to 18 months of treatment. In that period eight patients showed no evidence of active stone disease; three showed slight increase in the size of their old stone(s) and one patient formed one new stone. None of these patients developed any significant complications of the therapy. These findings support the view that pyridoxine in pharmacological doses is useful in the control of elevated urinary oxalate excretion in patients with recurrent renal oxalate calculi.
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PMID:Control of hyperoxaluria with large doses of pyridoxine in patients with kidney stones. 317 Jan 5

A 34-year-old woman developed a crystalline retinopathy after 2 years of inhalational abuse of methoxyflurane. After the woman developed renal failure, a renal biopsy showed multiple birefringent crystals in the renal tubular lumens, epithelial cells, and interstitium compatible with calcium oxalate. Multiple bright yellow-white crystals were deposited throughout the retina and at the level of the retinal pigment epithelium with a retinal arterial and periarterial predilection. This is the first reported case of methoxyflurane abuse with secondary hyperoxaluria in which there was a widespread retinal distribution of crystalline deposits, especially along the retinal arteries and arterioles.
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PMID:Calcium oxalate retinopathy associated with methoxyflurane abuse. 323 16

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

Despite the frequency and morbidity of nephrolithiasis in autosomal dominant polycystic kidney disease (ADPKD), this association has not been subject to a detailed study. One hundred fifty-one of 751 ADPKD patients seen at the Mayo Clinic between 1976 and 1986 had nephrolithiasis. Seventy-four had passed calculi or had stones surgically removed. Stone analysis was available in 30 patients: uric acid, calcium oxalate, calcium phosphate, and struvite were present in 56.6%, 46.6%, 20%, and 10%, respectively. Calculi were observed in 71 of 79 patients with excretory urograms available for review. Faintly opaque and bull's eye stones, probably containing uric acid, were present in 12.7% and 14.1% of these patients, respectively. Precaliceal tubular ectasia was observed in 15.5%. Ninety-seven patients had preserved renal function (serum creatinine less than 1.5 mg/dL) at the initial evaluation. Six were excluded because they had other known causes of stone disease. The most common metabolic abnormality in the remaining 91 patients was hypocitric aciduria (ten of 15 patients with measurements). The urine pH in the first voided morning specimens (5.66 +/- 0.05) was significantly lower than that of an unselected control population (5.92 +/- 0.03, P less than 0.001). Hyperuricosuria, hyperoxaluria, and hypercalciuria were observed in six of 32 (18.8%), six of 31 (19.4%), and three of 39 (9.7%) patients with preserved renal function. The composition of the stones, the frequency of hypocitric aciduria, and the low urine pH (possibly related to the defect in excretion of ammonia described in ADPKD), suggest that metabolic, along with mechanical, factors are responsible for the frequent occurrence of nephrolithiasis in this disease.
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PMID:The association of nephrolithiasis and autosomal dominant polycystic kidney disease. 335 68

The influence of a calcium-rich mineral water on urine crystallisation in patients with recurring kidney stones was investigated. A calcium and magnesium rich water like the one tested increases the calcium and magnesium content of the urine but decreases oxaluria even after a dietary oxalate load.
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PMID:[Prevention of the recurrence of urinary lithiasis: mineral waters with high or low calcium content?]. 343 28

Calcium oxalate uroliths are commonly called metabolic uroliths because they are sequelae of a variety of metabolic abnormalities that alter the composition of body fluids and urine. Factors incriminated in the etiopathogenesis of calcium oxalate urolithiasis include hypercalciuria, hyperoxaluria, and hyperuricosuria. The predominant type of calcium oxalate urolith encountered in dogs is the monohydrate form; however, the dihydrate form may also occur. Male dogs have been more frequently affected than female dogs. Medical therapy should be formulated with the goal of reducing urine concentration of calculogenic substances.
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PMID:Etiopathogenesis, clinical manifestations, and management of canine calcium oxalate urolithiasis. 351 99

Malabsorptive states are frequently associated with increased urinary oxalate excretion. The authors describe a 10-year-old girl with steatorrhea, hyperoxaluria, and a renal calculus in a single functioning kidney. Successful management of steatorrhea corrected both the chronic diarrhea and hyperoxaluria. Enteric hyperoxaluria is a well-known etiology of calcium oxalate urolithiasis in adults. Pediatricians caring for children with malabsorptive conditions should be aware of the risk of urinary calculus formation as a result of increased dietary oxalate absorption.
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PMID:Urolithiasis and enteric hyperoxaluria in a child with steatorrhea. 358 41

We used a xylitol load to test the two-carbon pathway to oxalate production in humans. Use of this pentose sugar caused a fourfold increase in glycolate excretion, indicating its suitability as a dynamic function test of two-carbon metabolism. However, despite this increase in glycolate excretion in 10 recurrent stone formers and six normal subjects, there was no concomitant increase in oxalate excretion in either group. By comparison, a sucrose load produced no increase in excretion of either glycolate or oxalate. In addition, when we studied four recurrent calcium stone formers on successive diets with various fat content, we found no correlation between high fat intake and increased glycolate or oxalate excretion. In summary, there was no evidence of abnormal fluxes through the two-carbon pathway to oxalate in recurrent stone formers, nor of hyperoxaluria as related to increased intake of sucrose or fat.
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PMID:Two-carbon oxalogenesis compared in recurrent calcium oxalate stone formers and normal subjects. 359 37

Twenty-two recurrent calcium stone formers had 24-h urinary oxalate excretions on their home diets which were significantly greater than those of 30 normal subjects (0.48 +/- 0.23 mmol/d; mean +/- SD compared with 0.31 +/- 0.11; P less than 0.01). The stone formers also demonstrated marked day to day variability in oxalate excretion indicating that a single normal urinary oxalate measurement did not exclude significant hyperoxaluria at other times. On a hospital diet containing 1000 mg calcium per day, urinary oxalate excretion fell significantly from 0.48 +/- 0.23 mmol/d to 0.32 +/- 0.12; P less than 0.01. As the urinary calcium excretion in and out of hospital was similar, it seems unlikely that low calcium intake at home was responsible for the hyperoxaluria. All patients had recurrent symptomatic stone disease and had been advised to avoid foods rich in oxalate. Whilst poor compliance is a possible explanation for the variability in oxalate excretion, we believe it is more likely that there is an inadvertent intake of oxalogenic precursors in their diet. As normal subjects do not demonstrate hyperoxaluria on similar home diets, stone formers may have a metabolic defect in the handling of these precursors.
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PMID:The variability and dietary dependence of urinary oxalate excretion in recurrent calcium stone formers. 366 88

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


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