The urinary transforming growth factor beta (TGF-β) excretion was measured in 33 patients including 10 with systemic lupus erythematosus (SLE), 8 with focal glomerular sclerosis (FGS), 9 with IgA nephropathy (IgAN), and 6 with membranous nephropathy (MN), and in 7 healthy subjects by enzyme-linked immunosorbent assay using a monoclonal antibody specific for TGF-β1+2+3. A significantly increased urinary TGF-β excretion was observed in FGS patients (555.5 ± 458.4 ng/mg Cr) as compared with normal controls (46.9 ± 43.9 ng/mg Cr) (p < 0.05) and a relative increase in SLE patients (96.4 ± 58.2 ng/mg Cr) and a decrease in MN patients (24.8 ± 13.3 ng/mg Cr). In contrast, there was no difference in TGF-β excretion between IgAN patients (54.1 ± 37.4 ng/mg Cr) and normal controls. A correlation between the amount of proteinuria and TGF-β was not found. As has been previously demonstrated in experimental studies, TGF-β may play a similar role in human glomerular diseases. The results obtained in this study raised the possibility that extracellular matrix might be produced by glomerular cells in vivo under the control of TGF-β and that TGF-β might act as a stimulator for the development of glomer