Urinary Excretion Of Oxalic Acid Research Articles

Review of the Role of Enteral Factor in the Development of Secondary Hyperoxaluria

Objectives: Discuss the role of the enteric factor in the hyperoxaluria development.
 Methods: Using the Internet and written materials, the relevant factors of enteral factor; hyperoxaluria; oxalotrophia; Oxalobacter formigenes; kidney stones, and with 36 references, were comprehensively analyzed and studied.
 Results: Under the condition of excessive intake of oxalate and its precursors, increased intestinal absorption of oxalate and imbalance of intestinal flora, resulting in increased urine oxalate and calcium oxalate crystal, which lead to hematuria, proteinuria, recurrent kidney stones and nephrocalcinosis.
 Discussion: Hyperoxaluria is a disease caused by metabolism disorder of oxalic acid and intestinal factors have significant influence on its progression. This disease can occur under the condition of excessive intake of oxalate and its precursors, increased intestinal absorption of oxalate and imbalance of intestinal flora, resulting in increased urine oxalate and calcium oxalate crystal, which lead to hematuria, proteinuria, recurrent kidney stones and nephrocalcinosis. Some patients may further progress to the AKI and CKD. With progressive decline in renal function, oxalate is reduced and deposits in the body can affect other tissues and organs. And adjustment of enteral factors is helpful for the treatment of hyperoxaluria.
 In this article we discuss the role of the enteric factor in the hyperoxaluria development. Hyperoxaluria is a metabolic disease characterized by excessive urinary oxalic acid excretion and calcium oxalate crystal deposition, whose intestinal factors affecting its onset includes the increased intake of oxalic acid and its precursors, the increased intestinal absorption of oxalate and the imbalance of intestinal flora, etc. Severe hyperoxaluria can lead to kidney stones. At present, the influence of intestinal factors on hyperoxaluria has become a research focus, this paper will give a comprehensive description of its related research.

Oxalic acid excretion after intravenous ascorbic acid administration

Ascorbic acid is frequently administered intravenously by alternative health practitioners and, occasionally, by mainstream physicians. Intravenous administration can greatly increase the amount of ascorbic acid that reaches the circulation, potentially increasing the risk of oxalate crystallization in the urinary space. To investigate this possibility, we developed gas chromatography mass spectrometry methodology and sampling and storage procedures for oxalic acid analysis without interference from ascorbic acid and measured urinary oxalic acid excretion in people administered intravenous ascorbic acid in doses ranging from 0.2 to 1.5 g/kg body weight. In vitro oxidation of ascorbic acid to oxalic acid did not occur when urine samples were brought immediately to pH less than 2 and stored at −30°C within 6 hours. Even very high ascorbic acid concentrations did not interfere with the analysis when oxalic acid extraction was carried out at pH 1. As measured during and over the 6 hours after ascorbic acid infusions, urinary oxalic acid excretion increased with increasing doses, reaching approximately 80 mg at a dose of approximately 100 g. We conclude that, when studied using correct procedures for sample handling, storage, and analysis, less than 0.5% of a very large intravenous dose of ascorbic acid is recovered as urinary oxalic acid in people with normal renal function.

Oxalic Acid as a Uremic Toxin

Oxalic acid (OA) is thought to be a uremic toxin that participates in the pathogenesis of uremic syndrome. The objectives of this study were to: (1) evaluate the plasma levels of OA in patients with chronic renal disease with various levels of glomerular filtration rate and after renal transplantation; (2) investigate the salivary secretion of OA and ascorbic acid in healthy subjects and in patients with chronic renal failure (CRF); (3) examine the influence of water and sodium diuresis and furosemide administration on the urinary excretion of OA and ascorbic acid in healthy subjects and in CRF patients without dialysis treatment; and (4) evaluate the influence of renal replacement therapy (RRT) on secondary hyperoxalemia in hemodialysis patients. This study was conducted at the Nephrological Department of P.J. Safárik University. Sixty-one patients with chronic renal disease, 64 CRF patients, 32 continuous ambulatory peritoneal dialysis (CAPD) patients, 15 hemodialysis patients, 21 patients after renal transplantation, and 15 healthy subjects were examined. Maximal water diuresis, diets with low (2 g/day) and high (15 g/day) sodium intake, administration of intravenous furosemide (20 mg), and renal replacement therapy (CAPD, hemodialysis, hemofiltration, and postdilution hemodiafiltration) were utilized in the study. In patients with chronic renal disease and those after renal transplantation, direct relationships between plasma OA and serum creatinine were found (r = 0.904 and 0.9431, respectively, P < .01). Despite a high level of plasma OA in uremic patients (23.1 +/- 10 micromol/L), there was no significant difference in salivary OA between control subjects (128 +/- 19 micromol/L) and CRF patients (135 +/- 24 micromol/L). The urinary excretion of OA during maximal water diuresis (from 37.5 to 110.3 micromol/4 hours) and after intravenous furosemide (from 34.5 to 66.7 micromol/3 hours) increased significantly, but was not affected by high intake of NaCl. The most significant decrease of plasma OA was observed during postdilution hemodiafiltration (63.3%). Our study indicates that renal replacement therapy is not effective for a permanent reduction of elevated plasma levels of OA.

Primary hyperoxaluria: Report of a patient with livedo reticularis and digital infarcts

Primary hyperoxaluria encompasses 3 rare genetic disorders of glyoxylate metabolism characterized by excessive urinary excretion of oxalic acid, resulting in oxalosis. Patients typically have recurrent calcium oxalate nephrolithiasis and nephrocalcinosis, leading to chronic renal failure and death from uremia. Oxalate can deposit in extrarenal sites such as the heart, walls of arteries and veins, bone, and skin. We report a patient who presented with acute renal failure and later experienced livedo reticularis and peripheral gangrene before the diagnosis of primary hyperoxaluria was established. A skin biopsy specimen demonstrated numerous characteristic elongate to diamond-shaped, radially oriented, pale yellow translucent oxalate crystals within the vessels, and vessel walls of the subcutaneous fat that were strongly birefringent under polarized light. (J Am Acad Dermatol 2002;46:S16-8.)

Influence of Water and Sodium Diuresis and Furosemide on Urinary Excretion of Vitamin B6, Oxalic Acid and Vitamin C in Chronic Renal Failure

Urinary excretion of vitamin B₆, oxalic acid and vitamin C was investigated in 15 healthy subjects during maximal water diuresis and in the group of 12 patients in polyuric stage of chronic renal failure without dialysis treatment receiving a diet containing high sodium chloride (15g/day). Urinary excretions of the same parameters were investigated in another group of 15 patients in polyuric stage of chronic renal failure without dialysis treatment after i.v. administration of 20 mg furosemide. Urinary excretion of vitamin B₆, oxalic acid and vitamin C significantly increased during maximal water diuresis while during high intake of sodium chloride the urinary excretions of these substances were not affected. The results suggest that urinary excretion of vitamin B₆, oxalic acid and vitamin C depends on the urinary excretion of water. Intravenous administration of 20 mg furosemide led to an increase of urinary excretion of vitamin B₆, oxalic acid and vitamin C in patients with chronic renal failure. The increased urinary excretion of vitamin B₆ and vitamin C is a new negative side effect of furosemide and increased urinary excretion of oxalic acid is a new positive side effect in patients with chronic renal failure.

Urinary excretion of oxalic acid in chronic renal failure and after kidney transplantation

Urinary excretion of oxalic acid in chronic renal failure and after kidney transplantation

The quantitation of oxalate in amniotic fluid by ion-chromatography

Calcium oxalate is the predominant constituent of most kidney stones. The rare genetic disorder, primary hyperoxaluria, is characterized by the continuous excessive synthesis and urinary excretion of oxalic acid, leading to stone formation and renal insufficiency. The earliest measurement of oxalate in suspected cases of primary hyperoxaluria is advantageous and would lend support for continued analysis and eventual confirmation of the disease. Therefore, we quantitated oxalate levels in amniotic fluid (AF) using medium pressure ion-exchange chromatography. The mean concentration of oxalate in amniotic fluid was 1.67 mg/1 ± 0.8 (SD); (range 0.64 to 5.11 mg/l). The mean oxalate/creatinine ratio (O/C) was 0.23 ± 0.11 (SD); (range 0.07 to 0.53.) This ratio is similar to that found in the urine of infants less than 1 year (0.19 ± 0.10; n = 17). There was no significant difference between males and females in oxalate concentration or O/C ratio. Regression analysis showed no significant correlation of fetal age with oxalate, O/C or creatinine. Studies in 13 sets of di-amnionic twins showed no statistical difference in oxalate or O/C between twin A and B. This study demonstrates the ability to accurately quantitate oxalate in amniotic fluid by ion-chromatography, and suggests that this may have a potential application in the initial screening process for the prenatal detection of primary hyperoxaluria.

Transient hyperoxaluria after ingestion of chocolate as a high risk factor for calcium oxalate calculi.

In 6 male subjects the diurnal variation of urinary oxalic acid excretion was studied after ingestion of chocolate, a food stuff rich in oxalic acid. The ingestion of chocolate caused a striking but transient increase in urinary oxalic acid excretion due to its absorption in the upper gastrointestinal tract. The peak excretion rates occurred 2-4 h after the intake of the chocolate. The peak values were 235% of the fasting excretion rate in the trial with 50 g chocolate and 289% in the trial with 100 g chocolate and reached the amounts found in cases with primary hyperoxaluria. The administration of ranitidine had no influence on oxalic acid absorption. The transient hyperoxaluria observed seems to be an important factor for the formation of calcium oxalate calculi in patients on risk for stone disorders.

THE EXCRETION OF OXALIC ACID IN GOUTY PATIENTS: 121

Utilizing the very satisfactory HPLC procedure recently reported by Hughes et al. (1), we have determined the urinary excretion of oxalic acid in control subjects (aged 20 to 70 years) and in gouty patients (from 35 to 73 years), before and after allopurinol treatment. The urinary excretion in normal subjects was 27.5±1.89 mg/24h, in gouty patients 31.3±3.08 mg/24h before allopurinol, and 43.22±4.66 mg/24h after treatment. It is evident that there is no substantial difference between normal subjects and gouty patients, while allopurinol significantly increases (p<0.05) the urinary excretion of oxalic acid. Since allopurinol inhibits the incorporation of glycine into purine ribonucleotides, this increase suggests that the glycine might be channeled toward the formation of glyoxylate and oxalic acid in gouty patients (2).Results suggest that the behavior of urinary oxalic acid should be under constant control during allopurinol treatment. (1) Hughes H. et al. (1982) Anal. Biochem. 119, 1-3 (2) Dean D.M. et al. (1968) Clin. Sci. 35, 325-335

Urolithiasis in railroad shopmen in relation to oxalic acid exposure at work.

It is well known that the urinary excretion of oxalic acid is one of the main determinants for urinary stone formation. From 1950 to 1978 a saturated oxalic acid solution was used in a repainting and cleaning process for railroad cars in Norwegian railroad workshops. With the use of a questionnaire, the cumulative prevalence of urolithiasis-induced colic episodes was registered in the Sundland railroad depot. Forty-two (11.9%) out of 353 male workers not exposed to oxalic acid reported having had one or more such stone colic episodes. The corresponding figure for 15 individuals who had a very high exposure to oxalic acid was 8 (53.3%). Also workers in other departments, occasionally exposed to oxalic acid, had an increased stone colic prevalence rate, a finding suggesting a positive dose-response relationship. There was an increased frequency of stone colic episodes in the age group 40-69 years. Seven heavily exposed workers in the paint shop reported initial pollakiuria and slight dysuria during the exposure. The study indicates a causal relation between urinary stone formation in the investigated railroad shopmen and their exposure to oxalic acid at work.

Gas-chromatographic determination of urinary oxalate.

We describe a simple, rapid method for determining urinary oxalate: isolation by precipitation with calcium chloride and conversion to dimethyl oxalate, which then is measured by gas chromatography. To each sample, tracer amounts of 14C-labeled oxalic acid are added, to determine the analytical recovery of urinary oxalate. Analytical recovery of [14C]oxalic acid added to urine specimens ranged from 15 to 95% (mean, 80%), and corrected recovery, based on calculation isotope-dilution techniques, ranged from 98 to 100%. The urinary excretion of oxalic acid by 18 normal men, ages 23 to 43 years, ranged between 9 and 23 mg/24h, with a mean value of 16 mg; that by 68 patients with small-bowel bypass ranged from 60 to 210 mg/24 h, with a mean of 127 mg.

Primary Hyperoxaluria

Primary hyperoxaluria is a hereditary disease caused by an inborn error of glycine/glyoxalate metabolism. This study presents the results of a Scandinavian survey of patients with primary hyperoxaluria diagnosed and/or treated through the years 1967 to 1976. Altogether 17 patients, 13 males and four females, were reported. The age at onset of the disease varied between three months and 29 years and the age at diagnosis between eight months and 45 years. Ten of the patients were still alive at the end of 1976 at ages between 14 and 49 years. In diagnosing primary hyperoxaluria attention is paid to the simultaneous determinations of the urinary excretion of oxalic acid, glycolic acid and glyoxylic acid. None of the different therapeutic measures in primary hyperoxaluria have, so far, received extensive evaluation. At present, large doses of pyridoxine in combination with taurine seem worth further investigation with a larger number of patients.

The Effect of Calcium on Hyperoxaluria Following Jejunoileal Bypass in Morbid Obesity

In order to investigate the effect on urinary oxalic acid excretion, ten patients with jejunoileostomy for morbid obesity were treated with oral calcium. We found a statistically significant decrease. The investigation suggests that the oral administration of calcium alone is not sufficient, in a dosage of 900 mg daily, to normalize the urinary oxalate excretion. The indications for calcium therapy in this group of patients is discussed.

原発性過蓚酸尿症

A case of primary hyperoxaluria with calcium oxalate nephrolithiasis was presented.The patient, 24 years old male, was quite well until the age of 15 when he was diagnosed as having left renal stones with symptoms of colic pain and hematuria. At the age of 19, he was operated for pyelolithotomy under the diagnosis of right renal stones. Following this operation he passed multiple stones during 5 years. Finally he came to our clinic and was diagnosed as having left multiple renal stones and right nephrocalcinosis.The removed staghorn calculi from the left kidney by nephrolithotomy in March, 18th. 1977 was analysed as pure calcium oxalate monohydrate by infrared spectrophotomater. The histological examination of the biopsy specimen demonstrated multiple deposits of crystalline material in the renal tubules under the polarizing microscope.From these results the abnormal oxalate metabolism was suspected, so that the urinary excretion of oxalic acid was measured. His urinary excretion of oxalic acid was markedly elevated to 140mg/24hrs (167.5mg/gr creatinine), but the excretion was within normal range in his parents and relatives.According to these findings he was prescribed pyridoxal phosphate 180mg/day under the diagnosis of primary hyperoxaluria. However the treatment was not effective. At present he is on hemodialysis because of postoperative progressive renal deterioration.

蓚酸代謝異常と尿路結石

Twenty four hour urinary excretion of oxalic acid was compared among control group, calcium oxalate stone group, and calcium oxalate and calcium phosphate mixed stone group. Oxalic acid was measured by the Hodgkinson & Williams method (1972) and expressed as anhydrous oxalic acid per 1.73m2 body surface area. The value of each control or patient is the mean of three to five assays. The above three groups excreted 30.2±1.5 (S.E.) mg (n=31), 41.4±3.4 (S.E.) mg (n=15), and 37.5±2.2 (S.E.) mg (n=23), respectively. The differences between control group and the latter two groups were statistically significant (P<0.01).

Effect of succinimide and other drugs on oxalate excretion by rats.

Succinimide, phenyl lactate, n-heptanoate, oxamic hydrazide, 2-oxoglutarate and ethinyl oestradiol all failed to reduce the urinary excretion of oxalic acid in male Wistar and Sprague-Dawley rats. The

Urinary oxalate excretion in patients with urolithiasis.

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

1920. Getting rid of oxalate: Zarembski, P. M. & Hodgkinson, A. (1969). Some factors influencing the urinary excretion of oxalic acid in man. Clinica chim. Acta25, 1

1920. Getting rid of oxalate: Zarembski, P. M. & Hodgkinson, A. (1969). Some factors influencing the urinary excretion of oxalic acid in man. Clinica chim. Acta25, 1

Some factors influencing the urinary excretion of oxalic acid in man

The effects of diet and other factors on the urinary excretion of oxalic acid were examined in normal subjects and patients with calcium oxalate-containing renal stones. Oxalate excretion varied directly with urine flow, suggesting that the renal tubular reabsorption of oxalate is determined by passive diffusion. The intestinal absorption and urinary excretion of oxalate were increased by reducing the dietary intake of calcium and by the oral ingestion of EDTA. Oxalate excretion was increased by the ingestion of glycine, glutamic acid and purines, reduced by ethinyl oestradiol and unaffected by ammonium chloride, sodium bicarbonate or magnesium. A diurnal variation in oxalate excretion was observed which was more evident in patients with renal calculi than in normal subjects. The diurnal rhythm was abolished by fasting. Longer-term variations in oxalate excretion were also observed. Oxalate excretion was usually reduced in hypoparathyroidism and increased in hyperparathyroidism and idiopathic hypercalciuria. It is concluded that the absorption of both oxalic acid and calcium may be increased in patients with idiopathic hypercalciuria.

Depression of calcium absorption in parathyroidectomized rats.

ARTICLESDepression of calcium absorption in parathyroidectomized ratsBG Shah, and HH DraperBG Shah, and HH DraperPublished Online:01 Oct 1966https://doi.org/10.1152/ajplegacy.1966.211.4.963MoreSectionsPDF (906 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByTransport of Calcium1 January 2011Drug Therapy of Urinary Calculi and Prevention of RecurrenceMammalian 25-Hydroxyvitamin D-1α-Hydroxylase: Measurement and RegulationIntestinal Absorption of Calcium: Its Assessment, Normal Physiology, and Alterations in Various Disease StatesCalcium-dependent, parathyroid hormone-independent regulation of 1,25-dihydroxyvitamin DU. Trechsel, J. A. Eisman, J. A. Fischer, J. P. Bonjour, and H. Fleisch1 August 1980 | American Journal of Physiology-Endocrinology and Metabolism, Vol. 239, No. 2Intestinal Effects of Vitamin DClinical Investigations of Calcium MetabolismAdaptation of intestinal calcium absorption: Parathyroid hormone and vitamin D metabolismArchives of Biochemistry and Biophysics, Vol. 188, No. 1Mechanisms of Calcium Absorption: A ReappraisalElevated serum levels of 1α, 25-dihydroxycholecalciferol in lactating ratsNature, Vol. 267, No. 5612Adaptation to calcium deprivation in the rat: effects of parathyroidectomy.J T Pento, L C Waite, P J Tracy, and A D Kenny1 March 1977 | American Journal of Physiology-Endocrinology and Metabolism, Vol. 232, No. 3Intestinal calcium transport: Parathyroid hormone and adaptation to dietary calciumArchives of Biochemistry and Biophysics, Vol. 175, No. 1THE ROLE OF THE PARATHYROIDS FOR THE ADAPTATION TO A LOW CALCIUM INTAKE.15 August 2009 | Acta Pathologica Microbiologica Scandinavica Section A Pathology, Vol. 83A, No. 1The physiology of parathyroid hormoneClinics in Endocrinology and Metabolism, Vol. 3, No. 2Calcium uptake and phosphate removal during hemodialysis with variing dialysate calciumKlinische Wochenschrift, Vol. 52, No. 6CalciumRegulation of 25-Hydroxycholecalciferol-1-Hydroxylase Activity in Kidney by Parathyroid HormoneNature New Biology, Vol. 241, No. 110BIBLIOGRAPHYA mathematical model for calcium homeostasisThe Bulletin of Mathematical Biophysics, Vol. 34, No. 4Effect of Dietary Phosphorus on Calcium Metabolism in Intact and Parathyroidectomized Adult RatsThe Journal of Nutrition, Vol. 102, No. 9The Tissue Localization of Tritiated Parathyroid Hormone in Thyroparathyroidectomized RatsJournal of Biological Chemistry, Vol. 247, No. 7Physiology and chemistry of parathyroid hormoneClinics in Endocrinology and Metabolism, Vol. 1, No. 1Calcium Absorption in Health and Disease25-Hydroxycholecalciferol: A Hormonal Form of Vitamin DAn electron microscopic localization of calcium in the small intestine of normal, rachitic, and vitamin-D-treated ratsCalcified Tissue Research, Vol. 5, No. 1Calcium metabolism in pregnant ewes9 March 2007 | British Journal of Nutrition, Vol. 24, No. 3Some factors influencing the urinary excretion of oxalic acid in manClinica Chimica Acta, Vol. 25, No. 1Absorption of major minerals in the small and large intestines of the ruminant28 February 2007 | Proceedings of the Nutrition Society, Vol. 28, No. 1Some Aspects of the Intestinal Absorption of Calcium, with Special Reference to Vitamin DReview of biochemistry of the calcified tissuesThe Journal of the American Dental Association, Vol. 76, No. 6Measurement and Meaning of Calcium AbsorptionGastroenterology, Vol. 54, No. 2 More from this issue > Volume 211Issue 4October 1966Pages 963-966 Copyright & PermissionsCopyright © 1966 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1966.211.4.963PubMed5926586History Published online 1 October 1966 Published in print 1 October 1966 Metrics