title: The dynamics of urinary N-acetyl-β-D-glucosaminidase (NAG), a marker of renal tubular dysfunction, in patients with lupus nephritis undergoing oral prednisone therapy.
abstract: OBJECTIVE
  N-Acetyl-β-D-glucosaminidase (NAG), a marker of renal tubular dysfunction, is increased in patients with lupus nephritis. In addition to the toxic effects of proteinuria, patients with lupus nephritis may exhibit other factors that contribute to tubular dysfunction, such as pathogenic antitubular basement membrane antibodies. The aim of our study was to assess urinary NAG, proteinuria, and glomerular filtration rate (GFR) before treatment and after 7 and 30 days of oral prednisone therapy in patients with lupus nephritis.
  
  
  METHODS
  Ten patients with lupus nephritis, all females, mean age: 29.4 ± 10.17 years, were enrolled into the study. All the patients received oral prednisone 1 mg/kg. Twenty healthy subjects served as controls. We measured urinary NAG before treatment and after 7 and 30 days of oral prednisone therapy. Proteinuria, GFR, blood pressure, and side effects of therapy were also followed up. Urinary NAG was measured using the colorimetrical method and expressed as units per gram of creatinine (U/gCr). Statistical analysis (Wilcoxon signed ranks test and Wilcoxon rank sum test) was performed using SPSS 17.
  
  
  RESULTS
  In the 10 patients with lupus nephritis, urinary NAG before treatment was 16.9 ± 13.39 U/gCr (P = 0.005 compared with controls). NAG in controls was 1.73 ± 0.51 U/gCr. Proteinuria before treatment was 3.84 ± 1.93 g/24 h. The GFR before treatment was 50.48 ± 11.98 mL/min/1.73 m². After 7 days of prednisone, urinary NAG was 23.55 ± 25.25 U/gCr (P = 0.878 compared with baseline, and P = 0.02 compared with controls). Proteinuria was 2.94 ± 1.3 g/24 h (P = 0.005 compared with baseline), and the GFR was 58.11 ± 13.64 mL/min/1.73 m² (P = 0.005 compared with baseline). After 30 days of prednisone, urinary NAG was 11.77 ± 12.18 U/gCr (P = 0.203 compared with baseline, P = 0.022 compared with the value after 7 days of prednisone, and P = 0.01 compared with controls). Proteinuria was 1.73 ± 0.68 g/24 h (P = 0.005 compared with baseline, and P = 0.005 compared with the value after 7 days of prednisone), and the GFR was 67.49 ± 16.42 mL/min/1.73 m² (P = 0.005 compared with baseline and P = 0.009 compared with the value after 7 days of prednisone). Blood pressure measurements did not show any significant changes. No major side effects of steroid therapy were noticed.
  
  
  CONCLUSIONS
  Urinary NAG showed a significant reduction between 7 and 30 days of therapy. The reduction in urinary NAG set in later than the decline in proteinuria and the improvement in GFR. Further studies incorporating a longer follow-up are needed to observe whether the reduction in NAG persists upon continuation of prednisone therapy.
authors.affiliation: Division of Nephrology, University of Medicine and Pharmacy "V. Babes" Timisoara, Romania. gluhovschi@yahoo.com
authors.forename: Cristina
authors.initials: C
authors.lastname: Gluhovschi
authors.forename: Silvia
authors.initials: S
authors.lastname: Velciov
authors.forename: Adriana
authors.initials: A
authors.lastname: Kaycsa
authors.forename: Gheorghe
authors.initials: G
authors.lastname: Gluhovschi
authors.forename: Ligia
authors.initials: L
authors.lastname: Petrica
authors.forename: Roxana
authors.initials: R
authors.lastname: Marian
authors.forename: Gheorghe
authors.initials: G
authors.lastname: Bozdog
authors.forename: Florica
authors.initials: F
authors.lastname: Gadalean
authors.forename: Flaviu
authors.initials: F
authors.lastname: Bob
authors.forename: Daniel
authors.initials: D
authors.lastname: Cioca
authors.forename: Corina
authors.initials: C
authors.lastname: Vernic
mesh_terms: D000118:Acetylglucosaminidase / Q000652:urine*; D000284:Administration, Oral; D000293:Adolescent; D000328:Adult; D000893:Anti-Inflammatory Agents / Q000008:administration & dosage*; D015415:Biomarkers / Q000652:urine; D005260:Female; D005919:Glomerular Filtration Rate / Q000187:drug effects*; D006801:Humans; D007684:Kidney Tubules / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D008181:Lupus Nephritis / Q000188:drug therapy* / Q000503:physiopathology / Q000652:urine*; D011241:Prednisone / Q000008:administration & dosage*; D011507:Proteinuria / Q000188:drug therapy / Q000503:physiopathology / Q000652:urine; D013997:Time Factors
chemical_list: D000893:Anti-Inflammatory Agents; D015415:Biomarkers; D000118:Acetylglucosaminidase; D011241:Prednisone