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

Severe oxalate nephropathy with end-stage kidney lesions was found in two pups of a litter of three Tibetan Spaniels. This histopathological finding strongly suggests a primary hyperoxaluria since there was no exposure to agents capable of producing secondary hyperoxaluria. Primary hyperoxaluria has not been reported as a spontaneous disease in the dog, although it is a well-known, but rare, inherited metabolic disease of man.
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PMID:Oxalate nephropathy in a Tibetan spaniel litter. A probable case of primary hyperoxaluria. 239 49

In normal adults the urinary excretion of oxalate rarely exceeds 0.5 mmol/24 hours-1 despite dietary and seasonal fluctuations of intake and absorption. Hyperoxaluria may be encountered in a number of disease states because of increased absorption of dietary oxalate or derangements of metabolism (Table 1). More unusually, hyperoxaluria may arise from one of three inborn errors of metabolism, i.e., the primary hyperoxalurias. The most common, primary hyperoxaluria type I (PHI), is recessively inherited; it will be discussed in detail in this paper. Primary hyperoxaluria type II, caused by a deficiency of D-glycerate dehydrogenase (EC 1.1.1.29), has a similar clinical pattern of disease, but has been described in only a very few families. More recently, another idiopathic form of hyperoxaluria has been defined (type III). It is likely that this form results from a primary defect in oxalate absorption in the absence of any morphologically or functionally definable intestinal disease; a satisfactory response to dietary restriction of oxalate, along with the use of thiazide diuretics, has been described.
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PMID:Perspectives in the assessment and management of patients with primary hyperoxaluria type I. 249 26

The medical history of a 42-year-old patient with primary hyperoxaluria type I is presented. Primary hyperoxaluria was suspected after renal transplantation, when oxalate deposits were found in a biopsy of the kidney graft. Diagnosis of type I hyperoxaluria was confirmed by the finding that significantly increased amounts of glycolic acid and oxalic acid were excreted. Treatment of the patient with 500 mg pyridoxine daily resulted in a decrease of the excretion of oxalate to normal values.
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PMID:Recurrence of nephrocalcinosis after renal transplantation in an adult patient with primary hyperoxaluria type I. 249 56

Renal calcifications have been described in very low birth weight (VLBW) infants, and diuretic drug-associated hypercalciuria is believed to play a role in the pathogenesis of this lesion. Hyperoxaluria is an important cause of renal stone formation in children and adults. Because parenteral nutrition solutions contain the oxalate precursors ascorbate and glycine, the relationship between total parenteral nutrition administration and oxalate excretion in VLBW infants was examined. Administration of approximately 0.5 g of total parenteral nutrition protein per kilogram per day to VLBW infants was associated with an increased urinary oxalate concentration and an increased urinary oxalate to creatinine ratio, when compared with VLBW infants receiving a glucose and electrolyte solution. A further increase in urinary oxalate concentration and oxalate to creatinine ratio was noted when total parenteral nutrition protein was increased to approximately 1.5 g of protein per kilogram per day. In VLBW infants who receive total parenteral nutrition, elevated urinary oxalate concentrations may develop and may be a factor in the pathogenesis of nephrocalcinosis in these infants.
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PMID:Urinary oxalate excretion by very low birth weight infants receiving parenteral nutrition. 250 54

Farnolith (a dietary fibre preparation) was given to normal patients (n = 6) with absorptive hypercalciuria type I (n = 6) and to one patient with renal hypercalciuria. Farnolith binds calcium and reduces calcium absorption in the intestines. In normal subjects, the urine and serum parameters of calcium metabolism (total and ionized calcium, 1.25-dihydroxy-vitamin D) were unchanged. In absorptive hypercalciuria type I, a significant decrease in calcium excretion was achieved; oxalate excretion decreased as well. Low PTH values normalized; vitamin-D metabolites were not affected. In renal hypercalciuria, PTH and 1.25 DHCC were increased, whereas hypercalciuria persisted. Our investigations show that Farnolith is a reasonable treatment for absorptive hypercalciuria. Calcium homeostasis is rendered normal by Farnolith without producing secondary hyperoxaluria as sodium cellulose phosphate. Patients with primary renal calcium leakage and secondary hyperparathyroidism should not be treated with Farnolith.
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PMID:[Studies of calcium metabolism in normal persons and patients with hypercalciuria in relation to therapy with the dietary fiber preparation Farnolith]. 253 20

Male Sprague-Dawley rats were challenged with various hyperoxaluric agents including ammonium oxalate, hydroxy-L-proline, and ethylene glycol. All treatments resulted in increased urinary oxalate. Associated with hyperoxaluria was an increase in urinary levels of renal enzymes, gamma-glutamyl transpeptidase, N-acetyl-beta-glucosaminidase, and alkaline phosphatase. Most of the rats did not demonstrate any significant change in urinary levels of beta-galactosidase. There was a highly significant positive correlation between urinary oxalate and N-acetyl-beta-glucosaminidase.
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PMID:Urinary enzymes and calcium oxalate urolithiasis. 257 Jan 67

An organic marine hydrocolloid (OMH) charged with calcium ('Ox-Absorb') was studied in vitro for oxalate binding and in patients with enteric hyperoxaluria to investigate oxalate excretion and the inhibitory activity on crystal formation of the urine. In-vitro experiments showed complete binding of oxalate to OMH. In clinical studies in nineteen patients with intestinal disorders and stone formation, urinary oxalate excretion was significantly lower during OMH treatment than off treatment. The activity product index of calcium oxalate was reduced on treatment. A pronounced rise in the inhibitory activity of urine was seen in two patients with very low pretreatment values. Most patients experienced virtual normalisation of bowel function, and in those with severe stone formation there was substantial clinical improvement. It is concluded that OMH has the capacity to bind oxalate in vitro and to reduce urinary oxalate excretion. These observations suggest a new promising treatment for enteric hyperoxaluria.
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PMID:Treatment of enteric hyperoxaluria with calcium-containing organic marine hydrocolloid. 257 Sep 57

Jejunoileal bypass (JIB) has been widely performed for treatment of excessive obesity. Formation of calcium oxalate stones is a common side effect. Since, under physiological conditions, the intestinal absorption of calcium and that of oxalate are interrelated, intestinal oxalate and calcium absorption were measured in the present study by isotope techniques in 19 JIB patients and 20 healthy controls. The JIB patients showed pronounced hyperoxaluria and markedly increased absorption of oxalate, with a urinary excretion of 14C-oxalate of 29 +/- 19% (controls 6.2 +/- 3.7%; p less than 0.001). There was a strong correlation between the intestinal absorption and urinary excretion of oxalate in the JIB patients (r = 0.72; p less than 0.001). Furthermore, their oxalate kinetics was altered, with continued urinary excretion of 14C-oxalate for up to 48 hours. The JIB patients also had reduced calcium absorption (36 +/- 9.1% vs. 47 +/- 9.0%; p less than 0.001) and patients with malabsorption of calcium and low urinary calcium had the highest intestinal absorption and urinary excretion of oxalate. It is concluded that hyperoxaluria in JIB patients is due to a significant extent to hyperabsorption of oxalate.
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PMID:Intestinal absorption of oxalate and calcium in patients with jejunoileal bypass. 259 24

Urinary oxalate concentrations were measured in 45 patients with quiescent Crohn's disease, four patients with chronic pancreatitis and five healthy subjects after a normal oxalate (150 g/day) diet, after a high-fat (150 g/day), normal oxalate diet and after and after a high-oxalate (500 mg/day) diet. Urinary oxalate concentrations were significantly (P less than 0.05) higher in patients with Crohn's disease and steatorrhoea, but not in those with chronic pancreatitis, after administrating a high-oxalate diet compared with healthy subjects. Mean oxalate values were 19.1 mg/24 h in controls compared with 65.8 mg/24 h in Crohn's disease patients. A direct correlation (r = 0.37, P less than 0.01) was established between faecal rats and urinary oxalate after oval oxalate load: this correlation (r = 0.43, P less than 0.01) is closer when only patients with Crohn's disease are considered. The study, therefore, confirmed a correlation between steatorrhoea and hyperoxaluria in patients with Crohn's disease; however, the high percentage of false positive results limits the use of urinary oxalate concentrations as a reliable indicator of lipid malabsorption. It is concluded that, at present, measurement of urinary oxalate cannot be recommended as a valid alternative to the Van de Kamer method for diagnosing lipid malabsorption.
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PMID:Urinary oxalate recovery after oral oxalic load: an alternative method to the quantitative determination of stool fat for the diagnosis of lipid malabsorption. 262 29

This article reviews the mechanisms involved in the synthesis, absorption, excretion and transport of oxalic acid, and the factors controlling these processes in man. The clinical syndromes associated with hyperoxaluria and recurrent calcium oxalate stone disease are reviewed, including new studies that raise the possibility of a generalized oxalate transport abnormality in some patients with renal stone disease. The important role of oxalate in the determination of calcium oxalate solubility in patients with calcium oxalate stone disease is emphasized and future directions for research in the prevention of recurrent calcium oxalate stone disease are discussed.
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PMID:Oxalate synthesis, transport and the hyperoxaluric syndromes. 264 33


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