Enteric and Other Secondary Hyperoxalurias

Rampton, D S; Sarner, M.

doi:10.1007/978-1-4471-1626-4_7

Cited by 2 publications

(8 citation statements)

References 77 publications

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“…Oxalate is the end product of vitamin C (ascorbic acid) metabolism 9. Glycolate is an intermediate in this process.…”

Section: Discussionmentioning

confidence: 99%

“…Glycolate is an intermediate in this process. It would be expected that if hyperoxaluria were the result of increased metabolic activity then glycolate excretion in urine would be raised 9. On the other hand if hyperoxaluria were secondary to increased uptake then an increase in urinary glycolate would not be expected.…”

Section: Discussionmentioning

confidence: 99%

“…Pyridoxine has been used to reduce urinary oxalate in mild metabolic hyperoxaluria 15. As noted, vitamin C is a source of oxalate9; vitamin C intake could therefore have altered oxalate excretion. Furthermore, high urinary concentrations of ascorbic acid have been shown to enhance stone formation 16.…”

Section: Discussionmentioning

confidence: 99%

“…Calcium oxalate stones have been found in other malabsorptive states8 9 in which there is thought to be enhanced uptake of oxalate leading to excessive urinary excretion of oxalate. Excess urinary oxalate has been reported in CF patients with stones,2 although the incidence of this finding in the CF population as a whole is not clear.…”

mentioning

confidence: 99%

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Oxalate and calcium excretion in cystic fibrosis

Turner

2000

Archives of Disease in Childhood

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Background-A patient with cystic fibrosis (CF) and repeated calcium oxalate renal stones prompted us to investigate other children for risk factors for this recognised complication of CF. Methods-Twenty four hour urinary excretion of calcium, oxalate, and glycolate was measured in children with CF and no symptoms of renal tract stones. Normal diet and treatments were continued. Results-In 26 children (aged 5-15.9 years) oxalate excretion was correlated with age; 14 of 26 children had oxalate excretion above an age appropriate normal range. There was a positive correlation between oxalate excretion and glycolate excretion. Mean calcium excretion was 0.06 mmol/kg/24 h with 21 of 24 children having calcium excretion below the normal range. Conclusions-Hyperoxaluria may reflect malabsorption although correlation between excretion of oxalate and glycolate suggests a portion of the excess oxalate is derived from metabolic processes. The hypocalciuria observed here may protect children with CF from renal stones.

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“…Oxalate is the end product of vitamin C (ascorbic acid) metabolism 9. Glycolate is an intermediate in this process.…”

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Oxalate and calcium excretion in cystic fibrosis

Turner

2000

Archives of Disease in Childhood

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“…Patients with gut disorders characterised by malabsorption of fat and/or bile acids excrete oxalate in the urine and are at increased risk of oxalate urolithiasis (Earnest, 1979;Laker, 1983 ;Rampton and Sarner, 1988). Enteric hyperoxaluria appears to result mainly from hyperabsorption of dietary oxalate and, apart from elimination of the underlying cause where possible, its treatment to date has depended largely on dietary measures (Earnest, 1979;Laker, 1983;Rampton and Sarner, 1988); however, the compliance of patients with advice to restrict oral intake of oxalate and fat is often poor.…”

mentioning

confidence: 99%

Failure of Allopurinol to Modify Urinary Composition in Enteric Hyperoxaluria

D’Cruz

Gertner²,

Kasidas³

et al. 1989

British Journal of Urology

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Conventional treatment of enteric hyperoxaluria (EHO) consists of dietary restriction of oxalate and fat and correction of its underlying cause whenever possible. Recent work suggests that allopurinol reduces the incidence of urolithiasis and the urinary excretion of both oxalate and uric acid in patients without intestinal disease. We have assessed the effect of allopurinol, 300 mg daily for 2 weeks, on urine biochemistry in patients with EHO due to small bowel Crohn's disease and/or resections. Compliance with treatment was confirmed by a fall in plasma uric acid in every patient. Allopurinol failed to alter 24 h urinary oxalate excretion or oxalate concentration. There were also no significant changes in the urinary excretion of glycollate (like oxalate, a breakdown product of glyoxylate), citrate, magnesium or calcium, each of which was at the lower end of the normal range before and during treatment with allopurinol. It appears unlikely that allopurinol will prove useful in the prevention of urolithiasis in patients with EHO.

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Enteric and Other Secondary Hyperoxalurias

Cited by 2 publications

References 77 publications

Oxalate and calcium excretion in cystic fibrosis

Oxalate and calcium excretion in cystic fibrosis

Failure of Allopurinol to Modify Urinary Composition in Enteric Hyperoxaluria

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