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)

In the literature there is a paucity of references on urolithiasis in children with spinal cord injury. In this paper 28 cases of urolithiasis in 97 children with spinal cord injury are analysed. An attempt is made to evaluate the role of hypercalcemia, hypercalciuria and urinary tract infection in the genesis of these calculi.
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PMID:Urolithiasis in children with spinal cord injury. 43 66

Renal ultrasound examination, performed following a urinary tract infection in a 4.5-year-old girl with triple X syndrome, showed multiple echogenic foci at the corticomedullary junction in both kidneys. She was asymptomatic but had hypertension with echocardiographic evidence of left ventricular hypertrophy. Computerised tomographic scan revealed foci of calcification in the kidneys, spleen and pancreas. On biopsy calcification was found in the internal and external elastic laminae of the superficial temporal artery and in the internal elastic lamina of a renal arcuate artery. Intimal fibrosis was mild and focal. No other arterial calcification was demonstrated radiographically or by ultrasound. Biochemical and hormonal profiles revealed no abnormality except hypercalciuria. The aetiology and prognosis of this child's condition are unknown. Although similar ultrasound and histological appearances have been described in pseudoxanthoma elasticum and in idiopathic arterial calcification of infancy, there is no evidence that the child has either of these conditions.
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PMID:Hypertension associated with diffuse small artery calcification: a case report. 148 46

In order to determine metabolic disorders in children with urolithiasis, 50 patients with urinary calculi were studied. Abdominal pain and/or haematuria were the most predominant symptoms. Surgical procedures were required in 22% of these children and urinary tract infection was observed in 34% of this group. Only 2 children had anatomical malformations of the urinary tract. Absorptive hypercalciuria (32%), renal hypercalciuria (34%) and uric acid hyperexcretion (24%) were the most common metabolic abnormalities in these children. We were unable to find an underlying metabolic abnormality in only 14% of the patients. These data suggest that appropriate metabolic study will allow rational management of children with urinary stones.
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PMID:Urolithiasis in childhood: metabolic evaluation. 153 41

Our primary objective was to test the hypothesis that a defect in acidification is more common in patients who have idiopathic calcium phosphate kidney stones than in those whose stones are formed mainly of calcium oxalate. Additionally, other risk factors might differ for these 2 stone types. Urine pH was measured serially over 24 hours, and along with ammonium and titratable acid, it was measured before and serially after ingestion of ammonium chloride in 3 groups of subjects: 24 patients with predominantly calcium phosphate stones, 30 patients with calcium oxalate stones, and 15 health non-stone-formers. Twenty-six parameters potentially related to stone formation and acidification were assayed on urines collected over 24 hours, and 15 parameters on blood. The data base was a computerized list of 5900 analyses of stones from patients living in Newfoundland. Patients not known by their physician to have had urinary tract infection, anatomical abnormality, hyperparathyroidism, or renal tubular acidosis were asked to participate in the study. Differences between means were considered significant if p values were less than 0.05 for F by analysis of variance and also less than 0.01 by t-test. In all patients with calcium oxalate stones and all non-stone-formers, urine acidified to pH less than 5.25, but in 8 of the 23 phosphate stone formers who completed the ammonium chloride study urine failed to acidify to pH less than 5.25. As all 8 had normal values for venous pH, total CO2, and chloride, they were considered to have incomplete renal tubular acidosis (IRTA). The 8 phosphate stone formers with IRTA had greater mean values for urine pH on all 9 specimens collected serially over 24 hours (all means greater than 6.2), and after administration of ammonium chloride (p less than 0.01), as well as lower mean values for urine titratable acid excretion (p less than 0.01), both after administration of ammonium chloride and in 24-hour urine samples, compared with the remaining phosphate stone formers whose urine acidified and the oxalate and non-stone-forming control groups. Nearly all the phosphate stone formers had 1 or more risk factors for stone formation, but with frequencies not significantly higher than those found in the oxalate group. Hypercalciuria and hypocitruria were the commonest, but increased oxalate or urate also occurred. Thus, idiopathic calcium phosphate stone formation can be associated with 1 or more of several risk factors, and, with the possible exception of those with IRTA, treatment should be similar to that given to patients with calcium oxalate stones.
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PMID:Comparison of patients with idiopathic calcium phosphate and calcium oxalate stones. 195 78

Biochemical evaluations were done two times for 29 outpatients with calcium stone disease, the first time within one month after surgical extraction or passage of stones and the second time two months or more later. Classification of the etiologic basis for the stone disease was the same after both tests in 27 patients. In the other 2 patients the diagnosis was changed from renal to absorptive hypercalciuria. Both of these patients had creatinine clearance rates less than 60 percent of normal during the first test. One also had multiple residual stones during both evaluations, and the second had a urinary tract infection during the first test that resolved with a normal creatinine clearance by the second test period. When nephrogenous cyclic adenosine monophosphate (cAMPn) assays were done on fasting specimens in these patients, the results were consistent with absorptive hypercalciuria. Almost all patients can be evaluated and placed in management programs within a few weeks after surgery. If cAMPn assays are not done, patients with decreased renal function secondary to residual stones or infection can be tested at a later time.
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PMID:Biochemical evaluation of calcium stone patients: how soon can it be done after stone surgery/passage? 217 93

We have evaluated the urinary excretion of promoting (calcium, phosphorus, uric acid, oxalate) and inhibiting (citrate, magnesium, glycosaminoglycans) factors of crystallization in subjects with idiopathic hypercalciuria and calcium urolithiasis and in a control group. The examined children had a free diet and were drug free for the last 2 weeks. They were not affected by malabsorption, D-RTA, urinary tract infection, or urinary tract malformation (factors interfering with urinary excretion of citrate and oxalate). In the patients with calcium urolithiasis, the daily urinary excretion of oxalate was significantly higher (p less than 0.01), and the urinary excretion of citrate was significantly lower (p less than 0.001) than in the subjects with idiopathic hypercalciuria and in the control group. Among the subjects with idiopathic hypercalciuria, those aged 4-9 years had a significantly reduced, though in the normal range, urinary excretion of citrate as compared with those aged 10-15 years (362 +/- 189 and 503 +/- 198 mg/g creatinine/24 h, respectively; p less than 0.01). Our data show that hypocitruria may play an important role in the pathogenesis of urolithiasis in children with idiopathic hypercalciuria. In these cases, the urinary citrate excretion was not inversely related to age, as has been suggested by other authors.
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PMID:Promoters and inhibitors of calcium urolithiasis in children. 225 56

In order to analyse the etiology of recurrent hematuria in childhood, we studied 250 children, referred to our Service (age: 6 mo-17 ys; 102 female and 148 male). They were submitted to the following protocol: urine analyses, uroculture, serum total and fraction complement, electrophoresis of hemoglobin, serum creatinine, BUN, 24h urinary calcium, uric acid and protein, oral calcium load test in children with hypercalciuria (UCa greater than 4mg/kg/day). Radiological evaluation and renal percutaneous biopsy was performed when necessary. The following diagnostic distribution was obtained: Alport syndrome, 19; Berger disease, 15; other glomerulopathies, 45; hypercalciuria, 67; uric acid hyperexcretion, 10; nephrolithiasis, 27; urinary tract infection, 14; renal malformation, 8; no diagnosis, 43. Based in these results, we conclude that appropriate investigation on recurrent hematuria, leads to determination of etiology in over 80% of cases.
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PMID:[Recurrent hematuria in children: study of 250 cases]. 248 11

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

A thorough metabolic evaluation of all staghorn stone patients seems justified, considering the results obtained by the study of 27 such cases. Pak's ambulatory screening test, slightly modified, was used. This allowed the finding of a hypercalciuria in more than 50% of the cases, a hyperuricosuria in 63% of the cases and a hyperoxaluria in one case out of five. A metabolic anomaly was not detected in two patients. Although urinary tract infection, present in 75% of the cases is essential to the genesis of a staghorn stone, the question raises whether metabolic anomalies are not the primary cause of the stone formation.
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PMID:[A study of the causes of staghorn calculi]. 281 90


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