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Glomerular microproteinuria in children treated with non-steroidal anti-inflammatory drugs for juvenile chronic
O Kordonouri1, C Dracou, F Papadellis
1Department of Pediatrics, Universitätsklinikum Rudolf Virchow, Berlin-Charlottenburg, Germany.
Insights
Children with juvenile chronic arthritis taking non-steroidal anti-inflammatory drugs (NSAIDs) show sub-clinical kidney damage. Glomerular protein markers in urine were elevated, indicating early signs of renal injury in these patients.
Area of Science:
- Nephrology
- Pediatric Rheumatology
- Pharmacology
Background:
- Juvenile chronic arthritis (JCA) affects children, often requiring long-term medication.
- Non-steroidal anti-inflammatory drugs (NSAIDs) are commonly used for JCA symptom management.
- Sub-clinical renal injury in children on NSAIDs requires sensitive detection methods.
Purpose of the Study:
- To investigate sub-clinical renal injury in pediatric patients with JCA treated with NSAIDs.
- To assess urinary excretion of glomerular and tubular markers in JCA patients on NSAIDs.
- To evaluate NSAID-induced nephrotoxicity in the absence of overt renal dysfunction.
Main Methods:
- Studied urinary excretion of albumin, transferrin, IgG (glomerular), and alpha 1-microglobulin (tubular) in 36 JCA patients on NSAIDs.
- Included 47 healthy children and 9 JCA patients not on NSAIDs as controls.
- Measured serum creatinine and urea nitrogen levels.
Main Results:
- Significantly elevated urinary excretion of glomerular markers (albumin, transferrin, IgG) in NSAID-treated JCA patients (p < 0.001).
- No significant difference in urinary tubular markers (alpha 1-microglobulin) or serum creatinine/urea nitrogen between groups.
- No correlation found between marker excretion and disease characteristics (onset, duration, activity).
Conclusions:
- NSAID therapy in JCA patients is associated with glomerular dysfunction in handling plasma proteins.
- Urinary protein and enzyme excretion assessment can detect early, sub-clinical renal injury in patients on NSAIDs.
- Monitoring urinary markers may be crucial for early detection and management of NSAID-induced nephrotoxicity in children.
Abstract:
The urinary excretion of selected glomerular (albumin, transferrin, and IgG) and tubular (alpha 1-microglobulin) protein and enzyme (N-acetyl-beta-D-glucosaminidase) markers was studied in 36 patients with juvenile chronic arthritis in order to investigate whether children receiving therapeutical doses of non steroidal antiinflammatory drugs (NSAIDs) and without clinical signs of gross renal dysfunction provide evidence of sub-clinical renal injury. Forty-seven age-matched healthy children as well as nine children with juvenile chronic arthritis but without NSAID therapy served as control groups. Although there was no difference between patients and controls regarding the serum creatinine and urea nitrogen levels, the urinary excretion of all three glomerular markers was significantly elevated in the patient group treated with NSAIDs (p < 0.001). In contrast, there was no difference between patients and controls concerning the urinary excretion of both tubular markers. Furthermore, no correlation was found between protein and enzyme excretion and the onset type, duration or activity of the underlying disease. Taken together, these data indicate that patients receiving NSAIDs display signs of glomerular dysfunction concerning the handling of plasma proteins. The systematic assessment of urinary protein- and/or enzyme-excretion may constitute a useful tool for the early detection and monitoring of otherwise subclinical renal injury in patients treated with NSAIDs.