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)

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

Six cases of tubular disorder of antenatal onset responsible for biological manifestations characteristic of Bartter syndrome and severe hypercalciuria are reported. In all six cases, severe hydramnios occurred during pregnancy between the 26th and 28th week after the last menstrual period. All six patients were born prematurely; gestational age ranged from 20 to 35 weeks. Major polyuria with dehydration occurred immediately after birth. The amounts of water and sodium needed to compensate urinary losses ranged from 280 to 370 ml/kg/day and 25 to 43 mmol/kg/d, respectively, during the first two postnatal months. Decreased serum potassium levels and increased plasma levels of renin and aldosterone were seen in all six patients. Increased urinary excretion of calcium was evidenced during the first postnatal week in three cases. Urinary calcium excretion in the six patients ranged from 15 to 30 mg/kg/d. Nephrocalcinosis developed in all six patients and two patients developed urinary lithiasis. One patient died at one month of age from necrotizing enteropathy. The five remaining patients gradually developed severe growth failure with measurements between 4 and 5.5 SDs below the mean. These five patients had evidence of hyperparathyroidism including increased serum levels of parathyroid hormone (5/5), increased serum alkaline phosphatase activity (4/5), and roentgenographic bone changes (1/5). Ionized calcium assays performed in three of the five patients disclosed low values (range 1.25-1.47 mmol/l; mean = 1.35; normal values = 1.42-1.62), although total serum calcium levels were normal or high (range 2.16-2.98 mmol/l; mean 2.61; normal values = 2.45-2.65) probably as a result of chronic dehydration.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Antenatal form of Bartter's syndrome]. 845 38

Our aim was to investigate the role of renal colic, a clinical condition characterized by excruciating pain, in the etiopathogenesis of irritable bowel syndrome (IBS). Two groups of patients were enrolled in the study. Group I consisted of 59 patients (33 male and 26 female) with a median age of 41.9 (18 to 58) years. The patients in group I were admitted to our clinic with urinary stone disease and with a medical history of acute renal colic. Group II consisted of 55 patients (25 male and 30 female) with a median age of 40.1 (18 to 56) years, complaining of urologic abnormalities other than stone disease. IBS was diagnosed using Rome criteria. Metabolic analysis for stone disease was performed on patients in group I. The incidence of five metabolic abnormalities--low urine volume, hypercalciuria, hyperoxaluria, hyperuricosuria and hypocitraturia--in patients with and without irritable bowel disease was investigated. IBS was found in 16 of the 59 patients (27.1%) in group I and in 6 of the 55 patients (10.9%) in group II. The difference was statistically significant (P < 0.05). Relative risk of developing IBS was 2.48 times higher in patients with urinary stone disease than in those without stone disease. There was no statistically significant difference in the metabolic analysis of patients with and without IBS in group I. IBS causes great suffering. Urinary stone disease should be considered as an etiological factor during management of IBS patients. In the presence of gastrointestinal symptoms, a patient with a medical history of acute renal colic might be referred to a gastroenterologist.
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PMID:Is there a relation between irritable Bowel syndrome and urinary stone disease? 1581 Jun 50