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Query: UMLS:C0020500 (hyperoxaluria)
 912 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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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PMID:Failure of allopurinol to modify urinary composition in enteric hyperoxaluria. 280 58

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.
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PMID:Transient hyperoxaluria after ingestion of chocolate as a high risk factor for calcium oxalate calculi. 291 54

The initial part of this presentation deals with the sensitivity of tests commonly used in the diagnosis of primary hyperparathyroidism. Total serum calcium levels often are normal in patients with small parathyroid adenomas but levels of serum ultrafilterable and/or ionized calcium usually are elevated in these patients. The recent introduction of improved radioimmunoassays for measurement of circulating parathyroid hormone has led to greatly improved sensitivity of this test for the diagnosis of primary hyperparathyroidism. However, measurement of total urinary cyclic adenosine monophosphate, even when expressed as a function of glomerular filtration rate, is an extremely insensitive test in patients who have parathyroid adenomas weighing less than 1 gm. Consequently, this test no longer is used for diagnostic purposes in our laboratory. Data relating to the prevalence and causes of hyperoxaluria in patients with idiopathic calcium oxalate stones also are presented. Hyperoxaluria (more than 450 mumol. per 24 hours) was found in 21 of 99 consecutive untreated male patients. Approximately a third of the patients with high normal or increased urinary oxalate excretion also have increased urinary glycolate excretion, which is indicative of increased endogenous oxalate production. This metabolic abnormality was unresponsive to pyridoxine administration but preliminary findings suggest that it may be corrected by restricting dietary protein.
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PMID:Clinical and laboratory approaches for evaluation of nephrolithiasis. 291 16

Spaceflight could provoke formation of kidney stones, in part by causing hypercalciuria and hyperphosphaturia. Applicants for spaceflight who have metabolic or environmental derangements to begin with might be particularly susceptible to stone formation in space. We, therefore, analyzed 24-h urine samples for stone-forming risk factors in 104 male applicants before their selection into the astronaut-mission specialist corps. The urinary environment was abnormally supersaturated with calcium oxalate in 25.0% of applicants, brushite in 36.5%, and monosodium urate in 66.3%, predisposing these applicants to crystallization of stone-forming calcium salts. This high level of supersaturation was caused by both "metabolic" and environmental disturbances. Thus, hypercalciuria was found in 11.5% of applicants, hyperoxaluria in 2.9%, hyperuricosuria in 18.3% and hypocitraturia in 5.8%. Environmental derangements were generally more prominent, as indicated by low urine volume of less than 2 L.d-1 in 84.6%, high urinary phosphate in 24.4%, and high urinary sodium in 10.6% of applicants. The results suggest that most of the abnormal stone risk factors disclosed among applicants for spaceflight programs were environmental in origin.
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PMID:Assessing applicants to the NASA flight program for their renal stone-forming potential. 293 Apr 28

An assay system for the measurement of the rate of Calcium Oxalate Monohydrate (COM) seed crystal growth in a metastable solution of calcium chloride and sodium oxalate containing traces of 14C-oxalic acid was used to assess the inhibitory activity of pyrophosphate (10(-5) M-10(-4) M), citrate (10(-4) M-10(-3) M) and urines of normal and pyridoxine deficient rats. Both pyrophosphate and citrate were strong inhibitors of COM crystal growth and caused a 50% decrease in crystal growth rate at 1.50 X 10(-5) M and 2.85 X 10(-4) M respectively. Normal rat urine strongly inhibited the COM crystal growth, while pyridoxine deficient animals showed a significant (p less than 0.01) decrease in mean inhibitory activity as compared to pair-fed controls. A lowered urinary inhibitory potential accompanied with hyperoxaluria and hypercalciuria, which is known to be associated with pyridoxine deficiency, may be a contributory risk of calcium oxalate crystallization and stone formation.
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PMID:Inhibition of calcium oxalate monohydrate (COM) crystal growth by pyrophosphate, citrate and rat urine. 302 39

Pyridoxine in doses of 250-500 mg daily by mouth was administered to 12 patients suffering from recurrent calcium oxalate renal calculi and idiopathic hyperoxaluria. This therapy decreased urinary oxalate excretion significantly (p less than 0.025) during up to 18 months of treatment. In that period eight patients showed no evidence of active stone disease; three showed slight increase in the size of their old stone(s) and one patient formed one new stone. None of these patients developed any significant complications of the therapy. These findings support the view that pyridoxine in pharmacological doses is useful in the control of elevated urinary oxalate excretion in patients with recurrent renal oxalate calculi.
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PMID:Control of hyperoxaluria with large doses of pyridoxine in patients with kidney stones. 317 Jan 5

A 34-year-old woman developed a crystalline retinopathy after 2 years of inhalational abuse of methoxyflurane. After the woman developed renal failure, a renal biopsy showed multiple birefringent crystals in the renal tubular lumens, epithelial cells, and interstitium compatible with calcium oxalate. Multiple bright yellow-white crystals were deposited throughout the retina and at the level of the retinal pigment epithelium with a retinal arterial and periarterial predilection. This is the first reported case of methoxyflurane abuse with secondary hyperoxaluria in which there was a widespread retinal distribution of crystalline deposits, especially along the retinal arteries and arterioles.
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PMID:Calcium oxalate retinopathy associated with methoxyflurane abuse. 323 16

Urinary oxalate is considered to play a crucial role in the formation of renal stones. In this respect hyperoxaluria constitutes a special problem, mainly because of the specific physicochemical properties of oxalate. The appropriate management of patients with this disorder must be based on a thorough understanding of the absorption, metabolism and excretion of oxalate. Different reasons for high oxalate excretion as well as analytical problems and our current therapeutic possibilities are covered in this review.
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PMID:Hyperoxaluria. 330 16

Hyperoxaluria and calcium oxalate lithiasis have a multifactorial genesis in bowel diseases. The augmented synthesis of oxalic acid in the liver is of minor importance. A diminished bacterial degradation is to asses up to day only hardly. The increasing absorption is of highest importance by deficient production of calcium oxalate in the intestinal tract and by increasing permeability of colonic mucosa above all in steatorrhoea or in patients with augmented calcium absorption. The crystallization of calcium oxalate in the urine is promoted by shortage of vitamin A, citrate, zinc or magnesium.
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PMID:[Pathogenesis of hyperoxalurias and calcium oxalate calculi in intestinal diseases]. 331 5

Despite the frequency and morbidity of nephrolithiasis in autosomal dominant polycystic kidney disease (ADPKD), this association has not been subject to a detailed study. One hundred fifty-one of 751 ADPKD patients seen at the Mayo Clinic between 1976 and 1986 had nephrolithiasis. Seventy-four had passed calculi or had stones surgically removed. Stone analysis was available in 30 patients: uric acid, calcium oxalate, calcium phosphate, and struvite were present in 56.6%, 46.6%, 20%, and 10%, respectively. Calculi were observed in 71 of 79 patients with excretory urograms available for review. Faintly opaque and bull's eye stones, probably containing uric acid, were present in 12.7% and 14.1% of these patients, respectively. Precaliceal tubular ectasia was observed in 15.5%. Ninety-seven patients had preserved renal function (serum creatinine less than 1.5 mg/dL) at the initial evaluation. Six were excluded because they had other known causes of stone disease. The most common metabolic abnormality in the remaining 91 patients was hypocitric aciduria (ten of 15 patients with measurements). The urine pH in the first voided morning specimens (5.66 +/- 0.05) was significantly lower than that of an unselected control population (5.92 +/- 0.03, P less than 0.001). Hyperuricosuria, hyperoxaluria, and hypercalciuria were observed in six of 32 (18.8%), six of 31 (19.4%), and three of 39 (9.7%) patients with preserved renal function. The composition of the stones, the frequency of hypocitric aciduria, and the low urine pH (possibly related to the defect in excretion of ammonia described in ADPKD), suggest that metabolic, along with mechanical, factors are responsible for the frequent occurrence of nephrolithiasis in this disease.
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PMID:The association of nephrolithiasis and autosomal dominant polycystic kidney disease. 335 68


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