Familial hyperoxaluria

Daniels, Richard A.; Michels, R. P. J.; Aisen, Philip; Goldstein, Gilbert

doi:10.1016/0002-9343(60)90116-9

Cited by 31 publications

(6 citation statements)

References 40 publications

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“…Smith and Williams also reported modest reductions in urine oxalate excretion in four patients during administration of 100-150 mg of pyridoxine per day (4). However, pyridoxine administration, even in the larger doses, has frequently been without significant effect (2,5,6,7). Recently Lynwood Smith at the Mayo Clinic has reported very encouraging results with the combined use of pyridoxine and orthophosphates which prevented progression of nephrolithiasis and the deterioration of renal function in this disease (8).…”

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“…In primary hyperoxaluria, only 2-5% of dietary oxalate is excreted in the urine so that restriction of dietary oxalate has relatively little effect on oxalate excretion (9,10). Because 40% of urinary oxalate is derived from glycine there have been unsuccessful attempts to reduce the availability of glycine by restricting dietary protein (2,9,10) or by administering sodium benzoate to trap glycine by the formation of hippurate (5,10,11). The feeding of D-amino acids to compete with glycine for D-amino acid oxidase has also been unsuccessful (4,12).…”

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Reduction of Urinary Oxalate Excretion in Primary Hyperoxaluria by Diet

1981

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Primary hyperoxaluria is a rare, hereditary disorder due to increased endogenous production of oxalate and characterized by increased urinary excretion of oxalate, the formation of calcium oxalate stones, and the deposition of calcium oxalate in the renal parenchyma and in other tissues. In the past it usually led to progressive renal failure and death from uremia at an early age.Members of this Association including Doctor James B. Wyngaarden and Doctor Hibbard Williams have made important contributions to our understanding of normal oxalate metabolism and the pathogenesis of primary hyperoxaluria. To provide a background to my presentation I shall briefly review the highlights of the current state of knowledge. Oxalic acid, a dicarboxylic acid, is a useless metabolic end product normally excreted in the urine in quantities not exceeding 50 mg per day. Of this amount, approximately 30% is derived from the absorption of dietary oxalate and a similar quantity is derived from the oxidation of ascorbic acid via metabolic pathways that are still not completely understood. The remaining 40% of urine oxalate is derived from the oxidation of its immediate precursor glyoxylate. In man, there are three known glyoxylate precursors, of which the two most important are glycine and glycolic acid. The third precursor a-keto-y-hydroxyglutarate, a compound formed during hydroxyproline catabolism appears to be relatively unimportant because urinary oxalate is not increased in conditions associated with increased collagen breakdown and the administration of large amounts of hydroxyproline to hyperoxaluric subjects failed to increase oxalate excretion.Hyperoxaluria may be either primary or secondary in nature. Secondary causes of hyperoxaluria include excessive dietary oxalate intake, enteric hyperoxaluria due to small bowel disease, pyridoxine deficiency, ethylene glycol poisoning and methoxyfluorane anaesthesia. Two forms

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Reduction of Urinary Oxalate Excretion in Primary Hyperoxaluria by Diet

1981

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“…It has also been suggested that primary hyperoxaluria and generalised oxalosis are two distinct entities, the former being a manifestation of renal malfunction and the latter being the true metabolic disturbance comparable to cystinuria and cystinosis (Daniels et al, 1960). Most, however, agree with Archer et al (1958) that both conditions are reflections of the same underlying defect, and that widespread oxalosis, the extreme manifestation of primary hyperoxaluria, is a tissue storage complication of excessive oxalate synthesis, comparable to urate deposition in tophaceous gout (Williams and Smith, 1972).…”

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Histopathological occurrence and characterisation of calcium oxalate: a review.

Chaplin¹

1977

J Clin Pathol

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“…A number of other agents, including ascorbic acid, d-glutamate, and histidine, have been given, also without apparent effect. A reduction in urinary oxalate has often followed ingestion of sodium benzoate (Archer et al, 1958a;Daniels, Michels, Aisen, and Goldstein, 1960), but the improvement lasted for only two weeks despite continued treatment. Presumably the increased conversion of glycine to hippurate associated with excess benzoate provokes a compensatory hypertrophy of mechanisms producing glycine.…”

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confidence: 99%