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

The causes of, and physiopathological factors underlying the most common metabolic disorders implicated in the formation of renal stones are reviewed. These include hypercalciuria, hyperoxaluria, renal tubular acidosis, cystinuria and disturbances of purine metabolism. Apart from metabolic disorders the risk of stone formation is also influenced by a low inhibitor activity in urine. Though some aspects in the pathogenesis of urolithiasis remain uncertain, the exact knowlege of important aetiological factors of stone formation is the basis of correct treatment and the prevention of recurrence of urinary calculi.
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PMID:[The evaluation of patients with urinary calculi discloses disturbances of metabolism in 75% of all cases (author's transl)]. 47 69

We report a retrospective study of 51 children who presented urolithiasis between 1980 and 1989 in our Hospital. Mean age was 7 years and the male:female ratio was 2. 1:1. A positive family history was found in 60% of cases. It was done metabolic evaluation in every case: hypercalciuria was found in 34% of cases. In 6% of cases there were hyperuricosuria. None of our patients presented hyperoxaluria, cystinuria or hypocitraturia. Abdominal echography was the most sensible an specific imaging technique of diagnosis. In 16 cases it was necessary a surgical procedure although most cases received only medical management. Four patients were treated with extracorporeal shock-wave lithotripsy. We emphasize the importance of metabolic evaluation. We report our own protocol of study and results.
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PMID:[Urolithiasis in childhood]. 177 65

Nephrolithiasis is a heterogeneous disorder, with varying chemical composition and pathophysiologic background. Although kidney stones are generally composed of calcium oxalate or calcium phosphate, they may also consist of uric acid, magnesium-ammonium phosphate, or cystine. Stones develop from a wide variety of metabolic or environmental disturbances, including varying forms of hypercalciuria, hypocitraturia, undue urinary acidity, hyperuricosuria, hyperoxaluria, infection with urease-producing organisms, and cystinuria. The cause of stone formation may be ascertained in most patients using the reliable diagnostic protocols that are available for the identification of these disturbances. Effective medical treatments, capable of correcting underlying derangements, have been formulated. They include sodium cellulose phosphate, thiazide, and orthophosphate for hypercalciuric nephrolithiasis; potassium citrate for hypocitraturic calcium nephrolithiasis; acetohydroxamic acid for infection stones; and D-penicillamine and alpha-mercaptopropionylglycine for cystinuria. Using these treatments, new stone formation can now be prevented in most patients.
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PMID:Etiology and treatment of urolithiasis. 196 46

Xydofon was applied to the treatment of 68 children suffering from different renal diseases associated with metabolic disorders. The latter ones involved oxaluria (28 children), uraturia (17 children), cystinuria (14 children), and phosphaturia (9 children). To appraise the action of xydofon, use was made of the indicators of membranolysis, cellular homeostasis of calcium, lipid peroxidation, and of the level of beta 2-microglobulin in urine. The results obtained indicate that xydofon can be used as an effective remedy for the treatment of children suffering from nephropathies associated with metabolic disorders.
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PMID:[Use of xidifon for prevention and treatment of nephropathies with metabolic disorders in children]. 234 37

The mechanism of stone formation in the urinary tract is reviewed. Diet, urinary tract infection and metabolic disorders account for the different epidemiological patterns of stone formation. The diagnosis and management of renal tract calculi are discussed. Calcium stones are associated with hypercalciuria, urine acidification defects, the use of furosemide in premature babies, hypercalcaemia, hyperoxaluria, hyperuricosuria, an alkaline urine and hypocitraturia. Uric acid stones occur in acid urine, from increased purine synthesis with lympho- or myeloproliferative disorders or from several inborn errors of purine metabolism which can also cause xanthine or dihydroxyadenine stones. Cystinuria, inherited as an autosomal recessive disorder is best treated with a low sodium diet, a fluid intake exceeding 40 ml/kg per day maintaining urine pH between 7.5 and 8 and, if necessary, with oral penicillamine. Oxalate stones occur in relation to diet, bowel disease and primary inherited defects in oxalate metabolism. Urinary tract infection causing struvite and carbonate apatite formation is the commonest cause of stones in Europe.
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PMID:Urolithiasis in children: current medical management. 270 15

Thirty-three children with urinary calculi were studied. In 12, a metabolic cause of calculi was identified (4 hyperoxaluria, 6 hypercalciuria, 2 cystinuria). In 14 children, lithiasis was associated with a urinary tract infection. No identifiable cause could be found in 7 children. A protocol for metabolic evaluation is proposed.
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PMID:[Urinary calculi in children. Etiologic survey]. 276 80

The increasing incidence of urolithiasis makes it important to report about 34 children with urolithiasis seen between 1976 and 1986 at the Department of Pediatrics, University Medical School Vienna. At the time of the first diagnosis 59 percent of the patients were less than 7 years of age; 62 percent of our patients were males. Recurrent chronic urinary tract infection in 32 percent, metabolic disorder (secondary hyperoxaluria 5, idiopathic hypercalciuria 3, cystinuria 2, hyperuricuria 2) in 27 percent were evaluated; in 13 patients the origin of calculi was idiopathic. Most infectious stones contained magnesium ammonium phosphate, most idiopathic stones calcium oxalate. In 21 patients (62%) surgical treatment, in one patient extracorporal shock wave lithotripsie was realized. Adequate metaphylaxis (general, dietetic, medicementous) can lower the rate of occurrence of stone formation.
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PMID:[Urolithiasis in pediatrics: analysis of 34 patients]. 368 52

The pathophysiologic consequences of renal function impairment and chronic renal failure among others result from the loss of excretory and regulatory functions of the kidneys. The role of the exchange of cellular hydrogen ions of tubular fluid in the reabsorption of bicarbonate and in the urinary excretion of titratable acid and ammonia (acid-base regulation) is outlined. The effects of decreased glomerular filtration rate on calcium and phosphorus homeostasis are discussed. De novo urolithiasis in these patients is uncommon. However, it is well recognized that they may form matrix stones with calcium oxalate inclusions. Of greater significance is the prophylaxis in those patients, in whom urolithiasis has been the cause of chronic renal failure. In these patients it is of importance to modify the drug dosage or to abandon the prophylaxis when it interferes with the metabolic changes of renal function impairment. Some agents require no modification, others minor or major modifications. Some are even contraindicated. Hazards of stone prophylaxis in chronic renal failure: Acidification - cave metabolic acidosis! Cave RTA! Antibiotic agents - special rules to prevent accumulation. Thiazides - contraindicated! Hypokalemia; hyperuricemia; cave HPT! Triamterene - contraindicated! Acetazolamide (cystinuria) - contraindicated. Spironolactone - contraindicated. Sodium-cellulose-phosphate - Hyperoxaluria, hypomagnesiuria , hyperphosphatemia, cave HPT. Orthophosphate - cave urinary infection, cave poor renal function, cave obstruction. Allopurinol - dose reduction advisable. Brenzbromaron - contraindicated.
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PMID:[Prevention of calculus recurrence in impaired kidney function]. 653 25

389 consecutive renal stone formers (275 males, 114 females) were investigated in an out-patient stone clinic. Renal tubular acidosis (RTA) was found in 83 patients (22%). Proximal RTA was twice as common as the distal tubular type. The acidification defects were exclusively of the incomplete form with normal basal blood acidbase status. Main diagnoses besides RTA were primary hyperparathyroidism (3.5%), medullary sponge kidney (3.5%), infection induced stones (3%), urate stones (2%), intestinal disorder (1.5%) and cystinuria (0.5%). The metabolic evaluation was mainly based on 24 h urine sampling on a free diet. In 248 patients (64%) no distinct abnormality was considered to be primarily responsible for stone formation. Clinical and biochemical analysis of these so-called idiopathic stone formers disclosed a male preponderance (80%) and, compared to a non-stone-forming control group, a higher urinary calcium excretion, yet with a considerable overlap between the two groups. Hyperuricosuria and hyperoxaluria were rare findings. The conclusion of the study is given as a proposal for clinical classification and ambulatory investigation of renal stone formers.
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PMID:Ambulatory diagnostic evaluation of 389 recurrent renal stone formers. A proposal for clinical classification and investigation. 684 37

To evaluate the incidence of heterozygous cystinuria in patients with primary and recurrent calcium oxalate stone disease 24-hour urine samples from 140 patients were examined. The frequency of heterozygous cystinuria in this study was only 1.4 per cent (2 patients). The frequency of other metabolic disorders was in accordance with other reports: hypercalciuria (32 per cent), hyperuricosuria (32 per cent) and hyperoxaluria (17 per cent).
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PMID:Heterozygous cystinuria and calcium oxalate urolithiasis. 687 77


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