GLOMERULAR MICROPROTEINURIA IN CHILDREN TREATED WITH NONSTEROIDAL ANTIINFLAMMATORY DRUGS FOR JUVENILE CHRONIC ARTHRITIS

The urinary excretion of selected glomerular (albumin, transferrin, an d IgG) and tubular (alpha 1-microglubin) protein and enzyme (N-acetyl- beta-D-glucosaminidase) markers was studied in 36 patients with juveni le chronic arthritis in order to investigate whether children receivin g therapeutical doses of non steroidal antiinflammatory drugs (NSAIDs) and without clinical signs of gross renal dysfunction provide evidenc e of sub-clinical renal injury. Forty-seven age-matched healthy childr en as well as nine children with juvenile chronic arthritis but withou t NSAID therapy served as control groups. Although there was no differ ence between patients and controls regarding the serum creatinine and urea nitrogen levels, the urinary excretion of all three glomerular ma rkers was significantly elevated in the patient group treated with NSA IDs (p<0.001). In contrast, there was no difference between patients a nd controls concerning the urinary excretion of both tubular markers. Furthermore, no correlation was found between protein and enzyme excre tion and the onset type, duration or activity of the underlying diseas e. Taken together, these data indicate that patients receiving NSAIDs display signs of glomerular dysfunction concerning the handling of pla sma proteins. The systematic assessment of urinary protein- and/or enz yme-excretion may constitute a useful tool for the early detection and monitoring of otherwise subclinical renal injury in patients treated with NSAIDs.