URINARY N-ACETYL-BETA-D-GLUCOSAMINIDASE AND BETA(2)-MICROGLOBULIN EXCRETION IN PRIMARY NEPHROTIC CHILDREN

Enzymuria and low molecular weight proteinuria reflect tubular damage and dysfunction, respectively. We examined urinary N-acetyl-beta-D-glu cosaminidase (U-NAG) and beta(2)-microglobulin (U-beta(2)M) excretion in 17 steroid-resistant and 39 steroid-sensitive children with nephrot ic syndrome whose glomerular filtration rates were within the normal r ange. Fourteen healthy children were taken as controls. U-NAG and U-be ta(2)M levels did not show a difference between the steroid-resistant and steroid-sensitive groups but were significantly higher in the neph rotic groups compared to the controls (p < 0.0001 and p < 0.01, respec tively). In the steroid-sensitive group, U-NAG levels were significant ly higher in patients in the relapse phase than in those in remission (p < 0.0001). This finding was also valid for U-beta(2)M excretion, bu t reached significance only for patients in remission who did not rece ive steroids (p < 0.01). There was a positive correlation between prot einuria and U-NAG and U-beta(2)M excretion in all patients (r(s) = 0.6 9, p < 0.001 and r(s) = 0.39, p < 0.001, respectively). In conclusion, massive glomerular proteinuria may cause a marked U-NAG excretion and a moderate urinary U-beta(2)M elevation independent of primary renal disease.