Glomerular microproteinuria in children treated with non-steroidal anti-inflammatory drugs for juvenile chronic arthritis.

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.