This study was designed to determine whether urinary excretion of IL-6 can be modified as a consequence of deterioration in renal tubular function. In patients with Kawasaki disease, IgA nephropathy and renal hypoplasia, IL-6 and beta 2-microglobulin were measured in the plasma and urine, and the excreted fractions of filtered IL-6 (FEIL-6) and beta 2-microglobulin (FE beta 2-microglobulin were calculated. Patients with renal hypoplasia had elevated FE beta 2-microglobulin which was associated with increased FEIL-6, and there was a significant relationship between these variables as the severity of renal hypoplasia increased. It was concluded that IL-6 in renal tubular fluid may be reabsorbed, catabolized as well as excreted by the renal tubule and that the level of urinary IL-6 excretion could be influenced not only by mesangial proliferation but also renal tubular dysfunction.