These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Urinary N-acetyl-beta-D-glucosaminidase and beta 2-microglobulin excretion in primary nephrotic children.
    Author: Calişkan S, Hacibekiroğlu M, Sever L, Ozbay G, Arisoy N.
    Journal: Nephron; 1996; 74(2):401-4. PubMed ID: 8893163.
    Abstract:
    Enzymuria and low molecular weight proteinuria reflect tubular damage and dysfunction, respectively. We examined urinary N-acetyl-beta-D-glucosaminidase (U-NAG) and beta 2-microglobulin (U-beta 2M) excretion in 17 steroid-resistant and 39 steroid-sensitive children with nephrotic syndrome whose glomerular filtration rates were within the normal range. Fourteen healthy children were taken as controls. U-NAG and U-beta 2M levels did not show a difference between the steroid-resistant and steroid-sensitive groups but were significantly higher in the nephrotic groups compared to the controls (p < 0.0001 and p < 0.01, respectively). In the steroid-sensitive group, U-NAG levels were significantly higher in patients in the relapse phase than in those in remission (p < 0.0001). This finding was also valid for U-beta 2M excretion, but reached significance only for patients in remission who did not receive steroids (p < 0.01). There was a positive correlation between proteinuria and U-NAG and U-beta 2M excretion in all patients (rs = 0.69, p < 0.001 and rs = 0.39, p < 0.001, respectively). In conclusion, massive glomerular proteinuria may cause a marked U-NAG excretion and a moderate urinary U-beta 2M elevation independent of primary renal disease.
    [Abstract] [Full Text] [Related] [New Search]