Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0451641 (urolithiasis)
 3,973 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A tubular renal damage induced by crystals in the renal tubuli can be the triggering primary but also secondary cause of stone formation. In 72 calcium oxalate stone patients (45 men, 27 women) N-acetyl-beta-D-glucosaminidase [NAG] excretion in 24h-urine was investigated. 48 healthy test persons (27 men, 21 women) served as a control group and helped to establish reference values. In order to find out a possible relation between NAG reference values and the risks of urolithiasis, lithogenous and inhibitory substances were determined in both groups. In the following, relative calcium oxalate supersaturation, representing a risk of urinary stone formation, was analyzed and compared to NAG excretion values. The threshold value of pathologic NAG excretion was determined in the group of healthy test subjects (mean value +/- 2 standard deviation) and was fixed at 4.2 U/d (women 3.06 U/d, men 4.24 U/d). In our investigations on NAG excretion significantly (p < 0.05) increased values were found in stone patients (4.43 U/d +/- 4.27) as compared to healthy test persons (2.13 U/d +/- 1.02). In the case of increased NAG excretion in stone patients there was a positive correlation between NAG excretion and increased phosphate, sulphate, uric acid, oxalate, and creatinine excretion. Only in female patients there was a relation between relative calcium oxalate supersaturation and NAG excretion values. As a result, NAG determination is considered to be an appropriate means of tracing a certain risk group within calcium oxalate stone patients.
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PMID:N-acetyl-beta-D-glucosaminidase excretion in calcium oxalate stone patients and its relation to the risk of stone formation. 900 22

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