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Analyses of Proteinuria, Renal Infiltration of Leukocytes, and Renal Deposition of Proteins in Lupus-prone MRL/lpr Mice
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Albuminuria and tubular markers in juvenile idiopathic arthritis

Ayla Kamburoğlu Göksel1, Lale Sever, Ozgür Kasapçopur

  • 1Department of Pediatric Nephrology and Rheumatology, Cerrahpaşa Medical School, Istanbul University, Turkey.

Pediatric Nephrology (Berlin, Germany)
|December 16, 2004
PubMed

Insights

Juvenile idiopathic arthritis (JIA) in children does not appear to cause permanent kidney damage, though active disease correlates with increased tubular enzymuria. Treatment with NSAIDs and SAARDs did not show significant differences in renal markers.

Area of Science:

  • Pediatric Nephrology
  • Rheumatology
  • Clinical Chemistry

Background:

  • Juvenile idiopathic arthritis (JIA) is a chronic condition in children.
  • Potential renal damage from JIA or its treatments (NSAIDs, SAARDs) requires investigation.

Purpose of the Study:

  • To assess renal damage in children with JIA.
  • To determine if damage is disease-related or treatment-related.

Main Methods:

  • Cross-sectional study of 45 JIA patients and 33 controls.
  • Measured urinary albumin/creatinine, NAG/creatinine, and beta(2)M/creatinine ratios.
  • Analyzed correlations with disease activity and treatment types.

Main Results:

  • No significant differences in urinary markers between JIA patients and controls.
  • Active JIA correlated with higher NAG/creatinine, linked to inflammation markers (ESR, platelets).
  • No association between markers and disease type, activity, or specific medications.

Conclusions:

  • Tubular enzymuria (NAG/Cr) increases during active JIA phases.
  • Permanent renal damage in JIA appears unlikely.
  • Disease activity, not medications, influences transient tubular enzyme elevation.

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