Lymphocyte adenosine deaminase activity in children with idiopathic nephrotic syndrome

Om P Mishra1, Jayant Ghosh, Ziledar Ali

  • 1Institute of Medical Sciences, Department of Pediatrics, Banaras Hindu University, Varanasi, India. opmpedia@yahoo.co.uk

Insights

Adenosine deaminase (ADA) activity is elevated in children with active nephrotic syndrome, particularly in relapsers. Levels normalize in long-term remission, indicating ADA

Area of Science:

  • Immunology
  • Pediatric Nephrology
  • Biochemistry

Background:

  • Cell-mediated immunity is crucial in idiopathic nephrotic syndrome (INS).
  • Adenosine deaminase (ADA) is a key enzyme in lymphocyte proliferation and differentiation.
  • Measuring ADA activity in serum and lymphocytes may offer insights into immune status in INS.

Purpose of the Study:

  • To evaluate serum ADA (S-ADA) and lymphocyte ADA (L-ADA) activity in children with INS.
  • To correlate ADA levels with disease activity, relapse frequency, and remission status.
  • To assess ADA as a potential biomarker for immune dysregulation in pediatric nephrotic syndrome.

Main Methods:

  • Adenosine deaminase activity was measured in serum and lymphocytes.
  • Study included 47 children with idiopathic nephrotic syndrome and 23 healthy controls.
  • Patients were categorized into active nephrotic syndrome, first attack, relapsers, frequent relapsers, and remission groups.

Main Results:

  • Significantly elevated S-ADA and L-ADA levels were observed in active nephrotic syndrome compared to controls.
  • ADA activity was highest in frequent relapsers and significantly higher in relapsers versus first-attack patients.
  • S-ADA normalized in remission, while L-ADA remained elevated but normalized in long-term remission.

Conclusions:

  • Adenosine deaminase activity is significantly altered in children with active nephrotic syndrome.
  • Elevated ADA levels correlate with disease activity and relapse frequency, suggesting immune involvement.
  • L-ADA may serve as a sensitive marker, showing changes even in the remission stage of INS.