Biochemical studies on the treatment of primary hyperoxaluria.

Gibbs, Dorothy A.; Watts, R. W. E.

doi:10.1136/adc.42.225.505

Cited by 31 publications

(8 citation statements)

References 19 publications

(13 reference statements)

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“…Although oxalate excretion in our patients was not so high as it was seen in patients with primary hyperoxaluria [1,4,12], our data suggest that even mild and intermittent hyperoxaluria may be the cause of re current calcium oxalate-containing renal stone formation.…”

Section: Discussioncontrasting

confidence: 61%

Urinary Oxalate Excretion in Patients with Urolithiasis

Revúsová¹,

Zvara²,

Gratzlová³

1971

Urol Int

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Urinary oxalic acid excretion was determined in 21 healthy people and 70 patients with renal stones. In the group of 31 patients with calcium oxalate-containing renal stones the mean value of urinary oxalate exretion was significantly higher than both in the normals and the patients with non-oxalate renal stones. Urinary oxalate excretion above the upper limit was found in 12 patients with calcium oxalate-containing renal stones (38.7%) and in one patient with radio-paque renal stones and nephrocalcinosis. In the patients with hyperoxaluria great variability in oxalate excretion was found. There was no relationship between urinary oxalate and calcium excretion and between urinary oxalate excretion and 24-hour volume of urine. It is suggested that there is relationship between the increased urinary oxalate excretion and recurrent calcium oxalate-containing renal stones formation in the investigated group of patients.

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Section: Discussioncontrasting

confidence: 61%

Urinary Oxalate Excretion in Patients with Urolithiasis

Revúsová¹,

Zvara²,

Gratzlová³

1971

Urol Int

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“…However, the administration of pyridoxine which facilitates the transamination of glyoxylate to glycine occasionally produces a worthwhile reduction in urine oxalate excretion. The best documented examples of a beneficial response are the cases described by Gibbs and Watts (2) and Will and Bijovet (3) in whom urinary oxalate excretion decreased by 50-70% during treatment with 600 to 1,000 mg of pyridoxine per day. 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).…”

mentioning

confidence: 99%

“…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).…”

mentioning

confidence: 99%

“…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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confidence: 99%

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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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“…Inhibition of oxidation of glyoxylate to oxalate is theoretically accomplished by inhibiting the three enzymes involved in this reaction, that is, xanthine oxidase, glycolate oxidase and LDH. However, neither allopurinol nor other inhibitors were proven to have significant effects on hyperoxaluria [57].…”

Section: Oxalate Biosynthesismentioning

confidence: 99%

The Primary Hyperoxalurias

Marangella

Petrarulo

Vitale

et al. 2001

Contributions to Nephrology

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The primary hyperoxalurias (PHs) are rare inherited diseases, characterized by elevated endogenous production of oxalate, and are essentially caused by defective detoxification of glyoxylate from body fluids [1]. The clinical consequences of this overproduction are due to three properties of oxalate: it is an end product of metabolism, it has a strong affinity for calcium, and the resulting salts have a very low solubility [2]. Fortunately, the body clearance of oxalate, which is quite solely accomplished by the kidney, is very efficient and, normally, plasma levels of oxalate are in the order of mol/l, with a daily production and excretion of 20 -50 mol [3][4][5].The main characteristics of oxalate turnover in man are depicted in table 1. At the physiological pH oxalic acid is virtually all dissociated and strongly binds to calcium. In aqueous solution the thermodynamic solubility product is in the order of few milligrams. Thanks to a very efficient renal elimination, plasma levels are kept well below the values corresponding to the limit of supersaturation [6]. However, this results in relatively high concentrations of oxalate in human urine, which are therefore quite always supersaturated with respect to calcium oxalate [7]. Indeed, oxalate is the main constituent of up to 70% of all renal stones [8].Most of the newly generated oxalate comes from endogenous sources, and only about 10% is absorbed in the intestine from dietary oxalate. However, the fraction of oxalate absorbed from the bowel varies greatly, and mostly depends on the presence of calcium in the diet [9]. The remaining 90% comes from endogenous sources, the principal dietary precursors being sugars, amino acids and ascorbate [10,11]. Whereas some doubt still remain about the actual contribution Schieppati A, Daina E, Sessa A, Remuzzi G (eds): Rare Kidney Diseases.

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Biochemical studies on the treatment of primary hyperoxaluria.

Cited by 31 publications

References 19 publications

Urinary Oxalate Excretion in Patients with Urolithiasis

Urinary Oxalate Excretion in Patients with Urolithiasis

Reduction of Urinary Oxalate Excretion in Primary Hyperoxaluria by Diet

The Primary Hyperoxalurias

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