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

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

On the basis of routine clinical and laboratory investigations, one or more probable or possible causes of stone formation were established in 27% of upper urinary tract and 98% of bladder stone patients. In the upper urinary tract, causes were usually found for triple phosphate and pure calcium phosphate stones and rarely for pure calcium oxalate stones. Except for cystine stones and largely for triple phosphate stones there was no definite correlation between the composition of stone and causes. Uric acid and urate stones were often not associated with obvious causes, but their demonstration should lead to further investigations. In a small group of recurrent calcium stone formers examined for hypercalciuria, hyperoxaluria, hyperuricosuria, and renal tubular acidosis, positive findings were noted for 65%, but there was no consistent correlation between these findings and the types of stone. Stone analysis is most useful in so far as it identifies or excludes triple phosphate, cystine, and uric acid/urate stones. This may be done by simple chemical analysis. Certain rare components may, however, be overlooked, as will details of stone structure, unless crystallographic methods are employed.
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PMID:Correlation between causes and composition of urinary stones. 634 79

Population based data on urinary excretion of various metabolites of pathological importance, Calcium, Magnesium, Sodium, Potassium, Oxalates, Citrates, Phosphates, Uric acid and urea have been collected from around three hundred children of the Quetta valley. The body weight was in the range of 11-50 kg and the age was in between 4-16 years. The urine excretion average was 987.5 +/- 452.5 ml per 24 hours. There was 11.5% incidence of hypercalciuria, 8.5% incidence of hyperuricosuria, 2.0% hyperphosphaturia, 2.5% hypomagnesuria, 3.5% hypocitraturia, 6.5% hypernatriuria, 43.5% hypokaliurea and 2.1% hyperoxaluria. Urea excretion average was 23.11 +/- 14.99 g per 24 hours. The study provided the basis for childhood reference pattern in urinary excretion of compounds related to various pathological conditions, in particular stone formation in this region.
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PMID:Population based data on urinary excretion of various metabolites in children of north western region of Pakistan. 1006 40

The first episode of nephrolithiasis provides an opportunity to advise patients about measures for preventing future stones. Low fluid intake and excessive intake of protein, salt and oxalate are important modifiable risk factors for kidney stones. Calcium restriction is not useful and may potentiate osteoporosis. Diseases such as hyperparathyroidism, sarcoidosis and renal tubular acidosis should be considered in patients with nephrolithiasis. A 24-hour urine collection with measurement of the important analytes is usually reserved for use in patients with recurrent stone formation. In these patients, the major urinary risk factors include hypercalciuria, hyperoxaluria, hypocitraturia and hyperuricosuria. Effective preventive and treatment measures include thiazide therapy to lower the urinary calcium level, citrate supplementation to increase the urinary citrate level and, sometimes, allopurinol therapy to lower uric acid excretion. Uric acid stones are most often treated with citrate supplementation. Data now support the cost-effectiveness of evaluation and treatment of patients with recurrent stones.
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PMID:Prevention of recurrent nephrolithiasis. 1059 18

Intestinal diseases may cause the formation of urinary stones through changes in the metabolism of oxalate, calcium, and uric acid. The oxalate that is excreted into urine comes from the catabolism of ascorbic acid and some amino acids or from intestinal absorption of food oxalate. Calcium is absorbed by the gut after the stimulation of active vitamin D and is excreted by the kidney under the control of the bone/parathyroid hormone axis. Uric acid is generated by the oxidation of exogenous and endogenous purine bases, is excreted by the kidney through glomerular filtration/tubular secretion, and is soluble in alkaline urine. Several data indicate that patients with inflammatory bowel diseases are at high risk of urinary stones containing calcium-oxalate salt or uric acid. Calcium-oxalate stones are caused by colonic oxalate hyperabsorption (secondary to intestinal dysfunction) or by parenteral nutrition. Uric acid stones are typical of patients with severe diarrhea and/or intestinal neostomy, that is, in patients with hyperconcentrated acidic urine. Relationships between malabsorptive intestinal diseases and urinary stones are less well defined. Preventive countermeasures are not the same for all disorders. Hyperoxaluria should be controlled by diets with a low content of lipids and oxalate but supplemented with calcium and probiotics. The presence of hyperconcentrated acidic urine should be controlled by correct hydration and administration of citrate.
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PMID:[Nephrolithiasis in patients with intestinal diseases]. 1826 17

Obesity is a significant health concern and is associated with an increased risk of nephrolithiasis, particularly in women. The underlying pathophysiology of stone formation in obese patients is thought to be related to insulin resistance, dietary factors, and a lithogenic urinary profile. Uric acid stones and calcium oxalate stones are common in these patients. Use of surgical procedures for obesity (bariatric surgery) has risen over the past two decades. Although such procedures effectively manage obesity-dependent comorbidities, several large, controlled studies have revealed that modern bariatric surgeries increase the risk of nephrolithiasis by approximately twofold. In patients who have undergone bariatric surgery, fat malabsorption leads to hyperabsorption of oxalate, which is exacerbated by an increased permeability of the gut to oxalate. Patients who have undergone bariatric surgery show characteristic 24 h urine parameters including low urine volume, low urinary pH, hypocitraturia, hyperoxaluria and hyperuricosuria. Prevention of stones with dietary limitation of oxalate and sodium and a high intake of fluids is critical, and calcium supplementation with calcium citrate is typically required. Potassium citrate is valuable for treating the common metabolic derangements as it raises urinary pH, enhances the activity of stone inhibitors, reduces the supersaturation of calcium oxalate, and corrects hypokalaemia. Both pyridoxine and probiotics have been shown in small studies to reduce hyperoxaluria, but further study is necessary to clarify their effects on stone morbidity in the bariatric surgery population.
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PMID:Stone formation and management after bariatric surgery. 2585 Jul 90