Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020438 (hypercalciuria)
 2,502 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Urinary uric acid excretion was assessed in 38 children to determine whether hyperuricuria was a risk factor in children with urolithiasis. Uric acid excretion (measured per deciliter glomerular filtration rate), and fractional excretion of uric acid were similar in 27 children with hypercalciuria and calcium oxalate urinary stones, in six children with idiopathic calcium oxalate urolithiasis, and in five with uric acid urolithiasis, of whom four were white boys and one was an Asian girl. One boy with a urate stone had cystinosis. Serum uric acid concentrations exceeded 6.0 mg/dl (360 mumol/L) in two children with hypercalciuria and in two patients with idiopathic calcium oxalate urolithiasis. None of the children with calcium urolithiasis had excessive urinary excretion of uric acid. In children with hypercalciuria, uric acid excretion did not change significantly when dietary sodium was increased from 1.0 to 5.0 gm/1.73 m2. We conclude that excessive urinary uric acid excretion is seldom an additional risk factor in children with calcium urolithiasis and that dietary sodium chloride does not have a strong influence on urinary excretion of uric acid in children with hypercalciuria.
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PMID:Uric acid excretion in children with urolithiasis. 258 28

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

We have investigated and treated 176 patients who were suffering from renal calculi. The stones contained calcium in 87% of patients, predominantly urate in 11%, and rarely contained magnesium ammonium phosphate or cystine. Of the patients with calcium stones, hypercalciuria was present in 75% and was identified in 57% by the measurement of the 24-hour urinary calcium excretion, and in a further 18% by a standardization calcium "fast-and-load" test. Nine patients were found to have primary hyperparathyroidism and were treated surgically. A further 21% were suspected to have normocalcaemic hyperparathyroidism, and metabolic studies are being developed to clarify this. The treatment of hypercalciuria included a low-calcium diet, and various combinations of a thiazide diuretic, phosphate supplements and sodium cellulose phosphate. Hypercalciuria was controlled in all compliant patients, and only two developed further stones. Hyperuricosuria was rarely the sole metabolic abnormality in patients with calcium stones, though this might reflect the referral pattern of the Unit. Uric acid stones were frequently, but not invariably, associated with hyperuricosuria and acid urine, and even large uric acid calculi dissolved with a combined therapy of high fluid intake, allopurinol and an alkalinizing agent. Surgical treatment was rarely required in these patients. A stone in the renal pelvis of one patient was removed percutaneously and did not require ultrasonic fragmentation. Modern methods of investigation and treatment have greatly improved the outlook for patients with recurrent renal calculi.
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PMID:Investigation and treatment of renal calculi. 404 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

A 20-year-old man with hypouricemia with markedly increased renal uric acid clearance is described. He also exhibited idiopathic hypercalciuria and lipoid nephrosis on hospital admission. Urate excretion was minimally suppressed by pyrazinamide and minimally increased after administration of probenecid, whereas it decreased after administration of benzbromarone. These results suggest that not only presecretory reabsorption, but also postsecretory reabsorption of urate was incompletely defective and indicate that the latter is more defective than the former. The relationship between hypouricemia and hypercalciuria or lipoid nephrosis in this case is not clear. However, since the hypouricemia persisted despite the remission of minimal change nephrotic syndrome, it appears that at least his nephrosis was incidental.
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PMID:Renal hypouricemia: incomplete combined defect. 793 74

The prevalence of arterial hypertension (HT) was investigated in 258 patients (171 m, 87 f, 22-68 years) with a history of primary stone disease. HT was detected in 64 patients (24.8%), with no difference between males (25.7%) and females (23.0%). The prevalence of HT by age was very similar to that of a general population, especially in the calcium stone group. The discriminant analysis demonstrated that the composition of stones, other than the age and body weight of the patients, were the main factors associated with HT. As far as the different kind of stone is concerned, the prevalence of HT was higher in patients with uric acid (17/37, 45.9%) and struvite stones (11/27, 40.7%) than in calcium stone formers (35/188, 18.6%) (chi 2 16.31, p < 0.001). The prevalence of hypercalciuria was higher in the calcium stone group than in uric acid or struvite stone patients (36.4 vs. 9.7 vs. 13.7%; chi 2 10.35, p < 0.01). Furthermore, the hypercalciuria showed a trend to be more prevalent in the untreated (47.0%) than in the treated (31.2%) hypertensives, or normotensives (35.1%). Uric acid stone formers were older, heavier and with higher triglycerides and uric acid plasma levels than calcium or struvite patients. Also the struvite stone formers were older than the calcium stone ones. Our data suggest that the prevalence of HT in kidney stone patients and particularly in calcium stone formers is similar to that of a general population. The role of hypercalciuria as the link for HT-urolithiasis association seems quite uncertain. Struvite and uric acid stone formers have higher risk for HT than calcium stone formers, probably due to the old age or to the associated metabolic abnormalities.
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PMID:Hypertension in kidney stone patients. 885 53

Hyperuricosuria with or without hypercalciuria amounted to about 23% of the possible cause of urolithiasis in my clinical experience. Approximately three forth of urolithiasis caused by hyperuricosuria was calcium oxalate stones and the rest was uric acid stones. Uric acid is one of the composition of urinary stones itself, but it has an activity of calcium oxalate stone formation. The hypotheses why the uric acid induced calcium oxalate stones were introduced. The preventive effect of allopurinol on the recurrent calcium oxalate stone formers was proved in our previous study which may revealed the urinary uric acid promoted calcium oxalate stone formation or masked the inhibitory activity of urinary macromolecular inhibitors. On the basis of above statement, I emphasize the importance of the treatment of hyperuricosuria in preventing urinary stones.
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PMID:[Hyperuricosuria and urolithiasis]. 897 4

Sonographic examinations as well as blood and urine chemistry tests were carried out in 4 neonates (3 mature, 1 premature) with transient renal failure, who were suffering from the effects of neonatal asphyxia of varying etiology. The first ultrasound examinations of the kidneys were performed within 24 hours after the hypoxic event. Simultaneously, blood and urine tests for parameters of renal function and purine metabolites were also carried out. Transient insufficiency of renal function could be detected in all cases with hyper-uricemia and hyper-uricosuria with no hypercalciuria. Ultrasonographic examinations showed hyper-echogenicity of the renal pyramids in all of the cases and hyper-reflectivity of the renal cortex in cases 2 and 4. In 3 cases, hyper-echogenicity appeared within 24 hours and disappeared in a short time, while in case 3 it could be detected from day 4 until day 14. These findings demonstrate, that the neonatal kidney is very sensitive to hypoxia and that hypoxic renal failure is accompanied by hyper-echogenicity of the kidneys. Uric acid is a possible cause of the renal hyper-echogenicity.
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PMID:The possible role of uric acid in renal hyper-echogenicity in neonatal hypoxic acute shock. 912 Jul 54

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


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