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 analysed material includes 100 children with urolithiasis treated in the Pediatric Clinic of the National Research Institute of Mother and Child in Warsaw between 1976 and 1978. Patients' age was from 3 months to 18 years. The analysed group included 51 boys and 49 girls. Urinary tract infection was found in 54 cases, i.e. 57,4% of the analysed material. The most common bacterial strains were those producing urease. They were detected in 48 children i.e. 88,9% of cases with urinary tract infection. Mostly these were bacteria of Proteus group--sporadically Pseudomonas aeruginosa and Staphylococcus albus. In the analysed patients urinary tract obstruction was observed in 36 children, i.e. 36% of cases. In 77% of the analysed material, localization of concrements was in upper urinary tract in 19% in the ureters and in 4% in the lover urinary tract. While in adult patients the most common compound of urinary stones was calcium oxalate, in children the most common stone compounds were phosphates (found in 38 cases i.e. 58,4% of the analysed material). The second frequent compound was oxalate found in 20 cases (30,7%). Less frequent compounds were uric acid and cystine. Performed study allowed to establish the cause of urolithiasis in 93 out of 100 examined children. Metabolic reasons of urolithiasis were found in 26 cases, i.e. 26% of the analysed material. They were as follows: idiopathic hypercalciuria--12 cases, uric acid urolithiasis--8 cases, primary hyperoxaluria--3 cases, cystinuria--2 cases, and incomplete acidosis of distal renal tubuli--1 case. Urolithiasis of probably metabolic origin was detected in 13 children (13%). Other reasons of urolithiasis in children were: infection (31%), idiopathic urolithiasis (17%) and others (6%). In 7 cases the reason of urolithiasis was not established.
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PMID:[Metabolic etiology of urinary calculi in children]. 717 91

The objective of this study was to determine the frequency of nephrocalcinosis and hypercalciuria in cystic fibrosis (CF) patients, and to search possible causes of this phenomenon. Forty-three CF children (24 boys, 19 girls; mean age 64.9 months, range 5 months-18 years) were included in this study. Plasma sodium, potassium, chloride, BUN, creatinine, calcium, phosphorus, magnesium, alkaline phosphatase; spot urine sodium, potassium, chloride, creatinine, calcium, magnesium; and serum 25-hydroxyvitamin-D levels were measured in all patients. Urine samples were examined for microscopic hematuria. Fractional sodium, potassium, chloride excretion and estimated glomerular filtration rate (GFR) were calculated. All patients underwent renal ultrasonography. Hypercalciuria, nephrocalcinosis and microscopic hematuria were detected in 15 patients (34.2%), 10 patients (23.2%) and two patients (5%), respectively. There was no significant but borderline correlation between 25-hydroxyvitamin-D levels and hypercalciuria (r: 0.308, p:0.05). There were no correlations between Shwachman clinical scoring system results and hypercalciuria (r: 0.221, p: 0.148) and age and hypercalciuria (r: -0.229, p: 0.135). Patients with chronic Pseudomonas colonization showed no hypercalciuria or nephrocalcinosis. There was no difference for plasma biochemical results, renal function tests, hypercalciuria and nephrocalcinosis between CF patients who had or had not experienced pseudo Bartter's syndrome (PBS) before. There was no relation between detected CF mutations of the patients and hypercalciuria and nephrocalcinosis. These results suggested that it is a primary abnormality of calcium metabolism in the kidney.
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PMID:Hypercalciuria and nephrocalcinosis in cystic fibrosis patients. 1507 70