Albuminuria and tubular markers in juvenile idiopathic arthritis


Pediatric Nephrology, vol.20, no.2, pp.154-158, 2005 (Journal Indexed in SCI Expanded) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 20 Issue: 2
  • Publication Date: 2005
  • Doi Number: 10.1007/s00467-004-1729-0
  • Title of Journal : Pediatric Nephrology
  • Page Numbers: pp.154-158


This study investigates whether renal damage occurs in children with juvenile idiopathic arthritis (JIA) either secondary to the disease per se or due to the side effects of non-steroidal anti-inflammatory drugs (NSAIDs) and slow-acting anti-rheumatic drugs (SAARDs) used in treatment. In this cross-sectional study, albuminuria, N -acetyl glucosaminidase (NAG), β2-microglobulin (β2M), and creatinine (Cr) levels were measured in urine samples of 45 patients (23 female, 22 male, 9.4±3.9 years) with JIA and a sex- and age-matched control group of 33 healthy children. The urinary albumin/Cr, NAG/Cr, and β2M/Cr ratios of children with JIA and of the control group did not differ statistically. No difference was noted between patient groups with different types of JIA (12 systemic, 18 polyarticular, and 15 oligoarticular JIA). JIA patients with active disease (n=16) had higher NAG/Cr values than patients with inactive disease (P=0.002). NAG/Cr levels correlated with erythrocyte sedimentation rate (r=0.66, P<0.001) and platelet count (r=0.61, P<0.001) and showed a slight correlation with the number of joints with active arthritis in children with polyarticular JIA (r=0.45, P=0.055). Neither β2M/Cr nor albumin/Cr ratios were associated with disease activity. No difference was noted between patient groups treated with different NSAIDs and SAARDs. In children with JIA tubular enzymuria increases during the active phase of the disease; however, it seems that permanent renal damage does not occur. © IPNA 2004.