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Query: UMLS:C0451641 (urolithiasis)
 3,973 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Idiopathic hypercalciuria (IH) in adults is recognized as a cause of urolithiasis. If IH is symptomatic, the symptoms are hematuria, renal colic, or obstructive uropathy with or without infection. In children, IH has been linked to the spectrum of urinary symptoms including hematuria, pyuria, dysuria, recurrent urinary infections, abdominal or suprapubic pain, proteinuria, and the frequency-urgency syndrome. Hematuria may appear prior to the appearance of stones, and thiazide therapy appears to prevent stone formation by decreasing urinary calcium excretion. This report describes an older adolescent with hematuria and flank pain. His urinary chemistry values were not consistently typical of IH, but a thiazide trial with withdrawal challenge was diagnostic. His case is remarkable because, though essentially an adult, his disease was typical of prepubertal disease. Adolescents with unexplained urinary symptoms should be evaluated for IH. The urinary calcium-creatinine ratio may not be elevated, and timed urinary calcium may be equivocal. In some cases a thiazide trial may be valuable and cost effective.
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PMID:Atypical idiopathic hypercalciuria in an adolescent. 318 67

Twelve children with urolithiasis or unexplained episodes of gross hematuria, hypercalciuria, and normal serum calcium levels were examined with an oral calcium loading test. Eight patients displayed elevated fasting urinary calcium excretion, consistent with renal hypercalciuria; four exhibited normal fasting calcium excretion, which increased excessively with calcium loading, suggesting hyperabsorption of intestinal calcium. Evidence of secondary hyperparathyroidism was detected in three children with renal hypercalciuria on the basis of urinary cyclic adenosine monophosphate (cAMP) excretion. Serum calcium concentrations obtained four hours after loading increased significantly in children with renal hypercalciuria and were directly correlated with fasting urinary calcium excretion. Among patients with renal hypercalciuria, serum calcium level was higher in patients with normal fasting cAMP excretion. These results suggest that hyperabsorption of intestinal calcium occurs in renal hypercalciuria and may account for the lower-than-predicted incidence of secondary hyperparathyroidism in these patients. Idiopathic hypercalciuria may arise from one fundamental metabolic disturbance with varying degrees of expression, rather than from two separate pathogenic mechanisms.
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PMID:Idiopathic hypercalciuria. Renal and absorptive subtypes in children. 632 Jun 35

An oral calcium loading test was performed on 55 patients with upper urinary tract stones to find absorptive or renal hypercalciuria. The mean urinary calcium excretion level of this patient group was significantly greater than that of a control group of 10 patients without abnormal upper urinary tract. Idiopathic hypercalciuria defined as more than 250 mg per day in males and more than 200 mg per day in females was observed in 13 patients; 4 patients with absorptive hypercalciuria, 6 patients with renal hypercalciuria and 3 patients of origin-unknown hypercalciuria. Five of the 6 patients with renal hypercalciuria had recurrent and/or multiple urolithiasis. From these results, this test was considered to be useful in the discrimination between absorptive and renal hypercalciuria.
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PMID:[Studies on an oral calcium loading test in upper urinary tract stone formers]. 648 63

Seven children with asymptomatic gross hematuria are described. Six had recurrent hematuria; one had a single episode. Occasional global glomerulosclerosis and/or mesangial electron dense deposits were present in the three patients in whom renal biopsy was performed; the changes were felt to be insufficient to account for the hematuria. None of the patients had urolithiasis or any significant urinary tract abnormality. One was an adopted child; a family history of urolithiasis was obtained in the other six. Idiopathic hypercalciuria was documented in six patients; the seventh subsequently passed a calcium oxalate calculus. One patient is 10 weeks of age at the time of this submission. Of the remainder, three patients received no specific therapy; renal calculi developed six months, six years, and eight years later. Three patients were treated with a thiazide diuretic soon after onset of hematuria and confirmation of idiopathic hypercalciuria; there was complete cessation of hematuria within five days with no recurrence as long as therapy was continued. We suggested that measurement of urinary calcium excretion as part of the initial evaluation of a child with gross hematuria may, in some cases, obviate invasive investigations and allow for effective therapy.
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PMID:The association of idiopathic hypercalciuria and asymptomatic gross hematuria in children. 729 44

We studied retrospectively 38 children who presented with urolithiasis between 1970 and 1977. The sex ratio was 1:1 and the mean age was 9.4 years. A positive family history was found in 36 per cent. Urinary tract abnormalities predisposing to infective urolithiasis was found in 7 children (18 per cent) but required voiding cystography for detection in 5. Hypercalcemia was found in 3 of 32 (8 per cent), while 28 of the 38 patients (74 per cent) had idiopathic urolithiasis. Idiopathic hypercalciuria was found in 5 of 13 patients (38 per cent) with idiopathic urolithiasis. Investigation of urolithiasis in children should include voiding cystography and measurement of urine calcium, as well as oxalate and uric acid, under home diet conditions.
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PMID:Pediatric urolithiasis in the 1970s. 735 29

Hypercalciuria is a rare biological symptom with multiple possible etiologies in children. Normal calcium excretion rate in children is defined as lower than 4 mg/kg per day, significantly higher values being observed in infants. When using urinary calcium: creatinine ratio, normal values are below 0.22 mg/mg in children, and below 0.6 to 0.8 mg/mg in infants. In our experience half patients with hypercalciuria have idiopathic hypercalciuria. Idiopathic hypercalciuria can be hereditary with a dominant autosomal mode of inheritance. Its pathophysiology is unclear, increased calcium intestinal absorption and impaired renal tubular calcium reabsorption being the two main underlying anomalies. Patients with hypercalciuria should be informed about the risk of urolithiasis and its possible prevention by a high water intake. In those patients with nephrocalcinosis or recurrent episodes of lithiasis, hydrochlorothiazide can be effective in reducing hypercalciuria. However, adverse effects of hydrochlorothiazide on serum lipids have been recently reported and make this treatment questionable in the long term.
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PMID:[Hypercalciuria: etiologies and treatment]. 918 9

Hyperuricosuria (HU), defined as a urinary acid excretion higher than 95 percent of normal values, is an important lithogenic factor, accounting for about 5-20% of recurrent hematuria in childhood. We prospectively studied 30 children (15 male, 15 female; aged 3 to 13 years old) with previously undiagnosed isolated hematuria and HU for 6 to 36 months. The family history of nephrolithiasis was positive in 40%. Idiopathic hypercalciuria (IH), UCa > 4 mg/kg/day, was not found initially, but was diagnosed after 6 to 24 months in 20% of the patients. The following treatments were utilized: restricted purine diet (13%), allopurinol (4%) and potassium citrate (1%). No specific treatment was given to 82% of the patients. Therapy normalized uricosuria with resolution of hematuria over 6-12 months. Thirteen percent and 6% of untreated patients developed urolithiasis after 6 and 12 months respectively. The data suggest that HU, like IH, is associated with hematuria. Furthermore, recognition of this association may prevent unnecessary, and in some cases, invasive diagnostic manoeuvres.
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PMID:Hematuria due to hyperuricosuria in children: 36-month follow-up. 940 12

Idiopathic hypercalciuria (IH) is defined as hypercalciuria that persists after correction of dietary inbalances and has no detectable cause. The excretion of urinary N-acetyl-beta-D-glucosaminidase (U-NAG), a marker of proximal tubular damage, has been previously reported as either increased or normal in children with IH. We evaluated U-NAG in 20 children (13 boys and 7 girls, mean age 10.3 years +/- 5.7 SD) with IH (urinary calcium excretion above 0.1 mmol/kg/24 hours, with no detectable cause) and with otherwise normal renal function tests. Ultrasound examination revealed urolithiasis (n=4) and nephrocalcinosis (n=1). The U-NAG values were evaluated in the spot urine collected from the second morning void and calculated as the urinary NAG/creatinine ratio (U-NAG/Cr) and expressed in nkat/mmol. The 24-hour urinary calcium excretion (U-Ca/24h) was assessed in a urinary sample from 24-hour collected urine and calculated in mmol/kg. The obtained results of U-Ca/24h and U-NAG/Cr were expressed as Z-scores. When compared to the reference data, the U-Ca/24h and U-NAG/Cr were significantly higher (p = 0.0004 and p = 0.006, respectively). There was no correlation between the U-NAG/Cr and U-Ca/24h (r = 0.18, p = 0.20). The U-NAG/Cr values were significantly higher in the 5 patients with urolithiasis/nephrocalcinosis, whether compared to the rest of the group (p = 0.02), or to the reference data (p = 0.01). The U-NAG/Cr activity was higher in 15 children without urolithiasis/nephrocalcinosis when compared to reference data (p < 0.01). There was no difference in U-Ca/24h between the children with and without urolithiasis/nephrocalcinosis (p = 0.58). These findings suggest that tubular impairment, as reflected by U-NAG/Cr, might occur in children with IH, especially in patients with urolithiasis/nephrocalcinosis. There doesn't seem to be a direct relationship between the U-NAG/Cr activity and the degree of calcium leakage.
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PMID:Renal tubular impairment in children with idiopathic hypercalciuria. 1695 19

Idiopathic hypercalciuria is the most important predisposing risk factor for calcium oxalate (CaOx) renal stone formation. We assessed the associations between spontaneous CaOx crystallization based on the Bonn Risk Index (BRI), urinary pH, calciuria, oxaluria, and citraturia in 140 Caucasian patients with hypercalciuria, aged 4-17 years, and compared the findings with those in 210 normocalciuric controls. Of the 140 hypercalciuric patients, 58 had renal stones, and 82 had recurrent erythrocyturia, renal colic, or urinary obstructive symptoms-but without stones. Urinary ionized calcium ([Ca(2+)]) levels were measured using a selective electrode, while the onset of crystallization was determined using a photometer and titration with 40 mmol/L ammonium oxalate (Ox(2-)). The calculation of the BRI was based on the [Ca(2+)]:Ox(2-) ratio. The BRI values were 12-fold higher in hypercalciuric children than in healthy controls, but no differences were found in the BRI between subjects with urinary stones and those with urolithiasis-like symptoms. An increased BRI suggested an association with hypercalciuria, lower urinary pH, hypocitraturia, and hypooxaluria. These data indicate that hypercalciuria is an important factor associated with increased urinary CaOx crystallization, although the causal pathways need further investigation. Determination of the BRI in children with hypercalciuria may improve the risk assessment of kidney stones.
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PMID:Spontaneous urinary calcium oxalate crystallization in hypercalciuric children. 1935 Feb 80

Patients with urolithiasis have been increasing in the world, especially morbidity of calcium nephrolithiasis has been increasing in the advanced countries. The changes in the environmental factors including alternation of diet are said to be associated with the increment of morbidity of kidney stone. Idiopathic hypercalciuria is one of the most important risk factor of calcium nephrolithiasis and is classified into absorptive, resorptive, and renal leak. Though the origins of these three types of hypercalciuria are different, increased bone resorption and increased calcium absorption from gut tend to be observed simultaneously. Not only genetic abnormalities in the proteins which are involved in calcium metabolisms but environmental factors such as high sodium intake and chronic acid load caused by increased ingestion of animal protein have been considered to be associated with increased urinary calcium excretion. Renal metabolisms of oxalate and phosphate which are important compositions of calcium containing stone, uric acid as a promoter and citrate as a inhibitor of nephrolithiasis are also described.
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PMID:[Renal calcium excretion and urolithiasis]. 2196 Feb 31


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