Practical Aspects of Oxalate Metabolism

Jeghers, Harold; Murphy, Rosemary

doi:10.1056/nejm194508162330704

Cited by 51 publications

(7 citation statements)

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“…(a) Exogenous oxalosis (i) Acute or chronic illness and even death may follow the ingestion of oxalic acid or one of the soluble oxalates (Jeghers and Murphy, 1945). The occurrence of such illness, particularly in children, as a result of eating rhubarb has been generally ascribed to oxalate toxicity (Crampton and Charlesworth, 1975) and, though most cases in England occurred in the first world war, when rhubarb leaves were recommended as a green vegetable substitute, there have been more recent instances (Tallqvist and Vaananen, 1960).…”

Section: Acquired Oxalosismentioning

confidence: 99%

“…'Oxalic acid is an example of a toxic substance that is consumed with impunity in small amounts in the daily food, yet when ingested in large amounts in pure form causes serious illness or death' (Jeghers and Murphy, 1945). Since that statement was made, a number of distinct clinical states involving the oxalate ion have been well defined, and it has been shown further that raised 'toxic' levels of oxalate may occur as a result of endogenous as well as exogenous processes.…”

mentioning

confidence: 99%

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Histopathological occurrence and characterisation of calcium oxalate: a review.

Chaplin¹

1977

J Clin Pathol

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Section: Acquired Oxalosismentioning

confidence: 99%

mentioning

confidence: 99%

Histopathological occurrence and characterisation of calcium oxalate: a review.

Chaplin¹

1977

J Clin Pathol

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“…It is well established that high-oxalate diets, such as those high in fruit juice, leafy greens, or tea, contribute to: (1) the risk of nephrolithiasis in a subset of recurrent stone formers, and (2) the risk of oxalate nephropathy in enteric hyperoxaluria [40–44]. More recently, the importance of Oxalobacter formigenes (O. formigenes) in preventing oxalate nephropathy has been increasingly reported.…”

Section: Discussionmentioning

confidence: 99%

Oxalate nephropathy in systemic sclerosis: Case series and review of the literature

Ligon

Hummers

2015

Seminars in Arthritis and Rheumatism

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Objective To increase awareness of oxalate nephropathy as a cause of acute kidney injury (AKI) among systemic sclerosis patients with small intestinal dysmotility and malabsorption, and to prompt consideration of dietary modification and early treatment of predisposing causes of oxalate nephropathy in this population. Methods Two cases of biopsy-proven oxalate nephropathy were identified among systemic sclerosis patients in the course of direct clinical care. Subsequently, a retrospective search of the Johns Hopkins Pathology databases identified a third patient with systemic sclerosis who developed oxalate nephropathy. Results Among the three patients with qualifying biopsies, all three had systemic sclerosis with lower gastrointestinal involvement. All three presented with diarrhea, malabsorption, and AKI. In two of the three patients, diarrhea was present for at least two years before the development of AKI; in the third, incidental oxalate nephropathy was noted three years before she developed AKI and extensive oxalate nephropathy in the setting of a prolonged mycobacterium avium-intracellulare enteritis. In one case, oxalate crystals were present by urinalysis months before diagnosis by biopsy, in the second, hyperoxaluria was diagnosed by urine collection immediately after biopsy, and in the third, oxalate crystals had been noted incidentally on post-transplant renal biopsy three years before the development of fulminant oxalate nephropathy. All three patients died within a year of diagnosis. Conclusions Patients with systemic sclerosis and bowel dysmotility associated with chronic diarrhea and malabsorption may be at risk for an associated oxalate nephropathy. Regular screening of systemic sclerosis patients with small bowel malabsorption syndromes through routine urinalysis or 24 hour urine oxalate collection, should be considered. Further studies defining the prevalence of this complication in systemic sclerosis, the benefit of dietary modification on hyperoxaluria, the effect of treating small intestinal bowel overgrowth with antibiotics, and the effectiveness of probiotics, calcium supplements, or magnesium supplements to prevent hyperoxaluria-associated renal disease in these patients, are warranted.

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“…19 Oxalosis is a consequence of oxalemia. Calcium oxalate is normally present in the urine in a super¬ saturated solution.…”

Section: Commentmentioning

confidence: 99%

“…Calcium oxalate is normally present in the urine in a super¬ saturated solution. 19 Carbohydrates, especially glycogen and starches, are considered the most important precursors of oxalate, while meats rich in connective tissue rank second. 19 Oxalosis is a consequence of oxalemia.…”

Section: Commentmentioning

confidence: 99%