Transforming growth factor-β (TGF-β) activity in urine of patients with glomerulonephritis is related to their renal functional and structural changes

Transforming growth factor-beta (TGF-beta) has been considered the principal cytokine involved in the pathogenesis of renal fibrosis. In the present study, we evaluated TGF-beta activity in occasional samples from 22 normal individuals and 29 patients (11; with focal glomerulosclerosis, 11 with membranous nephropathy, five with Berger disease, one with type I membranoproliferative glomerulonephritis and one with postinfectious glomerulonephritis) using a CCL-64 mink lung cell growth inhibition assay. A significantly increased urinary TGF-beta activity (reported in relation to urine creatinine, Ucreat. and median) was observed in patients with glomerulonephritis compared with normal individuals (P<0.01). The patients with Berger disease [median (Md) =9.96/10 mu g Ucreat.], membranous glomerulonephritis (Md= 7.23/10 mu g Ucreat.) and focal glomerulosclerosis (Md = 16.6/10 mu g Ucreat.) showed higher urinary TGF-beta than normal individuals (Md = 1.09/10 mu g Ucreat.) (P<0.01). We found a positive correlation between the TGF-beta activity in the urine of these patients and the incidence of segmental glomerulosclerosis (r=0.45, P<0.05) and their plasma creatinine levels (r=0.87, P<0.01). A negative correlation was observed between the TGF-beta activity in the urine of these patients and their creatinine clearance (r= -0.75, P<0.01). Our data suggest that measurement of urinary TGF-beta activity could be a useful non-invasive procedure for the evaluation of renal TGF-beta production, permitting the assessment of prognosis and the evaluation of therapeutic efficacy in patients with renal disease.