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

Dental and periodontal findings associated with primary hyperoxaluria in a 29-year old male patient are described. This is a rare, inherited, metabolic disease which results in excessive calcium oxalate synthesis. The predominant and early manifestation of hyperoxaluria is nephrocalcinosis which results in chronic renal failure. Widespread extrarenal deposits of calcium oxalate crystals, however, is a consistent finding. Extensive infiltration of crystals was noted in the pulps of the teeth, in the marrow spaces of the alveolar bone, in the gingival corium, and in the periodontal ligament. Crystalline calcium oxalate deposits in the periodontal ligament provoked a granulomatous foreign-body reaction. This resulted in aggressive external root resorption leading to pulp exposure and tooth mobility.
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PMID:Periodontal manifestations of hyperoxaluria and oxalosis. 273 33

The clinical features of a newly recognised inherited disease, primary hyperoxaluria in the cat, are reported. Affected cats developed acute renal failure between five and nine months old owing to the deposition of oxalate crystals in the tubules of the kidney. In addition to the signs attributable to kidney failure the affected animals became profoundly weak; there was evidence of denervation atrophy in skeletal muscle, and accumulations of neurofilaments were found in the proximal axons of the ventral horn cells and dorsal root ganglion cells of the spinal cord. Examination of urine from affected cats revealed L-glyceric aciduria and intermittent hyperoxaluria suggesting that the disease is a feline analogue of the human disorder, primary hyperoxaluria type 2. This supposition was confirmed by liver enzyme studies.
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PMID:Primary hyperoxaluria (L-glyceric aciduria) in the cat: a newly recognised inherited disease. 277 20

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

An 8-year-old boy who had suffered from recurrent stone formation since the age of 4 years, was admitted as an emergency due to anuria for a half day on November 20, 1986. Kidney-ureter-bladder film showed that the urethra was obstructed by a stone, and emergent cystoscopy was performed to remove it. He is the product of consanguinous marriage, his parents being first cousins. There was no family history of renal stone. Laboratory investigations showed hypokalemic, hyperchloremic metabolic acidosis. The ammonium chloride loading test revealed inability to acidify the urine and a markedly decreased excretion of titrable hydrogen ion and ammonium ion in the urine. These results indicate that this is a case of Type I renal tubular acidosis. His 24-hour urinary excretion of oxalate and glyoxylate were also markedly increased. There were no underlying causes leading to the development of secondary hyperoxaluria. These results also establish the diagnosis of Type I primary hyperoxaluria. The patient then received regimens of Polycitra 1ml/kg/day and Vitamin B6 50mg/day for 4 months. However, urinary stone developed again in this patient 4 months later. To our knowledge, Type I primary hyperoxaluria in association with Type I renal tubular acidosis has not been previously reported.
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PMID:Type I primary hyperoxaluria associated with type I renal tubular acidosis. 344 74

In order to find out whether hyperoxaluria can be demonstrated in patients on chronic (twice a week) haemodialysis, a group of 13 patients was investigated. These included one patient with proven primary hyperoxaluria, one suspected of having this disease and 11 patients in whom no information was available as to their oxalate metabolism. Oxalate concentrations in haemodialysate fractions and blood samples, taken before and after dialysis, were determined. The patient with primary hyperoxaluria had a plasma oxalate concentration before dialysis above 100 mumol/l and after dialysis above 25 mumol/l, while the oxalate concentration in haemodialysate at the start of dialysis was above 25 mumol/l and at the end above 10 mumol/l. The patient suspected of hyperoxaluria had similar values. Of the remaining 11 patients, one was shown to exhibit a transient hyperoxaluria, but the others showed a normal oxalate metabolism. A plasma oxalate/creatinine concentration ratio exceeding 0.1, and the calculated total quantity of oxalate removed by dialysis exceeding 2 mmol, also enabled a diagnosis of hyperoxaluria to be made. Hyperoxaluria can still be demonstrated in patients, who because of renal failure are subjected to haemodialysis. Measurements of oxalate in haemodialysate and plasma are valuable in cases where kidney transplantations are considered, especially when the particular patient exhibits hyperoxaluria.
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PMID:The determination of oxalate in haemodialysate and plasma: a means to detect and study 'hyperoxaluria' in haemodialysed patients. 370 74

Hyperoxaluria may result in diffuse deposition of calcium oxalate crystals in multiple organs. A patient with primary hyperoxaluria presented with peripheral ischemia on this basis. Computed tomography clarified the diagnosis and helped to direct the appropriate management.
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PMID:Vascular and soft tissue calcification in systemic oxalosis: CT diagnosis. 373 14

Pyridoxine (vitamin B6), given to patients with primary hyperoxaluria of type I, generally leads to a decrease in urinary excretion of oxalate owing to stimulation of conversion of glyoxylate to glycine instead of oxalate. It is not known, however, whether pyridoxine would equally influence hyperoxalurias of other origins, e.g. idiopathic or enteric. Two groups of patients were therefore given pyridoxine orally for 2 months (300 mg/d). Group 1 consisted of 10 idiopathic stone formers with mild hyperoxaluria of unknown origin. Group 2 consisted of 4 patients with enteric hyperoxaluria after intestinal bypass surgery. As a mean, enteric hyperoxaluria was not influenced by vitamin B6, which suggests that this disorder is the consequence of intestinal hyperabsorption of oxalate rather than of glyoxylate. In contrast, idiopathic hyperoxaluria was influenced by vitamin B6: urinary excretion of oxalate decreased in 8 patients out of 10 and became normal in 7. However, two patients did not respond to pyridoxine; both had concomitant severe hyperuricosuria (greater than 1 g/24 h), an observation suggesting that in these cases hyperoxaluria was of dietary origin. Four of the patients whose urinary excretion of oxalate became normal while on pyridoxine were followed up for 8 to 36 months after treatment: in all of them oxaluria remained normal. One whose oxaluria had returned to the upper normal limit was retreated after 2 years and again displayed a fall in urinary oxalate. It is concluded that pyridoxine given to idiopathic hyperoxalurics may correct the disorder, as in primary hyperoxaluria of type I; this is not the case in enteric hyperoxaluria. The mechanisms governing this sensitivity to vitamin B6 remain to be clarified.
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PMID:[Pyridoxine can normalize oxaluria in idiopathic renal lithiasis]. 379 70

This report describes studies performed over an 11 year period in a 13 year old girl with hyperoxaluria and calcium oxalate nephrolithiasis who did not have primary hyperoxaluria or any of the recognized causes of secondary hyperoxaluria. The patient also had increased urinary excretion of calcium and magnesium and hyperabsorption of dietary calcium and magnesium. It is suggested that the hyperoxaluria resulted from hyperabsorption of dietary oxalate secondary to hyperabsorption of dietary calcium. Hyperabsorption of dietary magnesium and increased urinary magnesium excretion have not previously been reported in this context. Stone formation ceased and urinary oxalate excretion gradually fell to normal during long term thiazide therapy but hyperoxaluria recurred when orthophosphate therapy was substituted for the hydrochlorothiazide. This is the first report of normalization of urine oxalate excretion during thiazide therapy in a patient with frank hyperoxaluria.
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PMID:Absorptive hyperoxaluria: a new clinical entity--successful treatment with hydrochlorothiazide. 395 21

We measured urinary oxalate and glycolate excretion before and during pyridoxine administration (2 to 200 mg per day) in four patients with primary hyperoxaluria. In two patients with type I primary hyperoxaluria, urinary oxalate and glycolate excretion fell markedly in response to a physiologic dose of pyridoxine of 2 mg per day and became completely normal when the dose was increased to 25 mg per day. In the other two patients, who had a different type of primary hyperoxaluria (normal urinary glycolate excretion), there was no response to 2 mg of pyridoxine per day. In one of these patients, doses of 25 and 50 mg per day were also ineffective, but a moderate reduction in oxalate excretion took place with 200 mg per day; in the other patient there was a moderate reduction in oxalate excretion with 25 mg of pyridoxine per day. Our findings suggest that the degree of hyperoxaluria in this disorder may be only slight or moderate if the patient has been ingesting a pyridoxine-rich diet or multivitamin tablets containing small amounts of pyridoxine. Our results also suggest that smaller doses of pyridoxine than those heretofore employed should be tried in patients with primary hyperoxaluria.
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PMID:Response to a physiologic dose of pyridoxine in type I primary hyperoxaluria. 397 85

We have measured glomerular filtration rate (GFR), extracellular fluid volume (ECF), oxalate distribution volume (OxDV), plasma oxalate concentration (POx.), plasma total clearance of oxalate (PCOx.), oxalate metabolic pool size [(OxDV) X (POx.)], renal clearance of oxalate (RCOx.), oxalate excretion, tissue clearance of oxalate (TCOx.) and tissue oxalate accumulation rate [(TOx.A) = (TCOx.) X (POx.)] in three patients with type I primary hyperoxaluria (hyperoxaluria with hyperglycollic aciduria) when they were taking pyridoxine and after discontinuation of the vitamin. Seven days after stopping pyridoxine the plasma oxalate concentration, oxalate metabolic pool size and the urinary excretion of oxalate had all increased between seven- and eight-fold in two of the patients. The third patient showed no changes on stopping pyridoxine. These results support the view that pyridoxine acts by reducing oxalate biosynthesis in some patients with type I primary hyperoxaluria. The possible biochemical basis for this effect is discussed.
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PMID:The effect of pyridoxine on oxalate dynamics in three cases of primary hyperoxaluria (with glycollic aciduria). 406 59


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