Urinary tubular enzyme excretion in children with nephrolithiasis and urolithiasis with hydronephrosis

Objective: Nephrolithiasis and urolithiasis are recurrent conditions associated with significant morbidity and economilc impact. Previous studies have suggested that cell- crystal interactions lead to tubular damage and/or dysfunction. To find further proof for these observations, a metabolic evaluation [including serum and urine biochemistry and urinary enzyme excretion] was done in children with nephrolithiasis and urolithiasis with hydronephrosis

Patients and Methods: This study included two groups: 10 normal children [controls] and 32 children with calcium oxalate urinary tract stones. The latter group was further subdivided into those with nephrolithiasis [n=12] and urolithiasis with hydronephrosis [n=20]. Levels of uric acid, oxalate, calcium, magnesium and inorganic phosphorus in 24-hour urine and serum were determined. Urinary N-acetyl-beta-D-glucosaminidase [NAG], beta-galactosidase [beta-GAL], beta-hexosaminidase [beta-Hex], angiotensin converting enzyme [ACE] and gamma glutamyl transferase [y-GT] levels were also determined colorimetrically

Results: Increases in urinary excretion of oxalate, calcium, magnesium and inorganic phosphorus were the major abnormalities found in stone forming patients. Elevated urinary NAG, beta-GAL, beta-Hex and ACE levels were also noted in patients compared with controls. Urinary excretion of oxalate, NAG, beta-GAL and ACE was significantly elevated in children with nephrolithiasis compared to those with urolithiasis and hydronephrosis

Conclusion: Abnormal urine biochemistry seems to have a role in the risk for urinary-tract stone formation in children. Hyperoxaluria can induce tubular cell injury mainly in proximal tubules, which is more pronounced in children with nephrolithiasis. The tubular injury manifested by enzymuria occurs before alteration of renal functions and blood biochemistry. Urinary tubular enzymes should be screened in children with urinary tract stones

Urinary N-acetyl-B-D-glucosaminidase, microalbuminuria, and microtransferrinuria as indicators of diabetic nephropathy

Urinary levels of total protein, albumin and transferrin [as estimates of glomerular function] and urinary N-acetyl-B-D-glucosaminidase [NAG] activity [as estimate of tubular function] were determined in 10 healthy control persons [GI] and in 40 insulin-dependent diabetic patients, 10 patients with clinical proteinuria [GIII] and the other 30 patients without clinical proteinuria [GII]. Group II was further subgrouped according to the duration of diabetes into three subgroups: GIIa [10 patients with duration of less than 2 years], GIIb [10 patients with duration of 2 to 10 years, and GIIc [10 patients with duration of more than 10 years]. The patients and controls were also investigated for fasting blood glucose, glycosylated hemoglobin and creatinine clearance. In diabetics with clinical proteinuria, urinary levels of total protein, albumin and NAG activity were significantly increased when compared with other groups. Also, urinary transferrin was only detected in this group. In diabetics without clinical proteinuria creatinine clearance was significantly increased in group IIa and IIb when compared with controls and in group IIb when compared with group IIc. There was a significant increase in microalbuminuria in group IIc when compared with the control, group IIa and group IIb. Also, urinary NAG activity was significantly increased in group IIc when compared with the control and group IIa. Urinary albumin and transferrin were found to be negatively correlated to the creatinine clearance in group III, while there was a positive correlation between urinary transferrin and urinary albumin and total urinary protein in the same group

Urinary N-acetyl-beta-D-glucosaminidase (NAG) in aminoglycoside nephrotoxicity.

Urinary N-acetyl-beta-D-glucosaminidase (UNAG) excretion was measured in 37 children before and during the treatment with aminoglycosides at the Department of Pediatrics, Ramathibodi hospital from July 1 to October 31, 1986. There were 20 males and 17 females whose ages ranged from 15 days - 15 years. Twelve were in postoperative status, 11 with respiratory tract disease, 11 with urinary tract disease and 3 in the miscellaneous group. Aminoglycosides were given alone in 11 patients, combined with cloxacillin in 14 and with other antibiotics in 12 patients. The duration of aminoglycoside given ranged from 5-27 days (mean +/- SD = 11.5 +/- 5.5 days). Clinical nephrotoxicity was detected in 12 patients (32.4%), of which 7 were males and 5 were females, 4 were less than 1 year old. It appeared 4-9 days (mean +/- SD = 5.8 +/- 1.6 days) after initiation of the treatment. Variation in age, sex, initial UNAG excretion and antibiotic combination were not associated with increased risk of nephrotoxicity. Thirty patients had elevated baseline UNAG excretion from 1-14 times higher than the normal value. UNAG excretion was increased 0.23-5.57 fold in all patients after 24 hours of treatment. In those with clinical nephrotoxicity, the enzymuria rose more than one fold in all of them (sensitivity 100%, specificity 68%, accuracy 78.4%) and this was detected 2-7 days (mean +/- SD = 3.8 +/- 1.6 days) prior to the rise of serum creatinine.(ABSTRACT TRUNCATED AT 250 WORDS)