Abstract
Urinary transforming growth factor-beta (TGF-beta) excretions were 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 7 healthy subjects by enzyme-linked immunosorbent assay (ELISA) using monoclonal antibody specific for TGF-beta1+2+3 A significantly increased urinary TGF-beta excretion was observed in FGS patients, 555.5±458.4ng/mgCr, than that of normal controls, 46.9±43.9ng/mgCr (p<0.05), and a relative increase in SLE patients, 96.4±58.2ng/mgCr, and decrease in MN patients, 24.8±13.3ng/mgCr. In contrast, there was no difference of TGF-beta excretion between IgAN patients, 54.1±37.4ng/mgCr, and normal controls. A correlation between the amount of proteinuria and TGF-beta was not found.
As has been previously demonstrated in experimental studies, TGF-beta may play a similar role in human glomerular diseases. Results obtained in this study raised the possibility that extracellular matrix (ECM) might be produced by glomerular cells in vivo under the control of TGF-beta, and that TGF-beta might act as a stimulator for the development of glomerulosclerosis.
