title: Steroid therapy and urinary transforming growth factor-beta1 in IgA nephropathy.
abstract: Transforming growth factor-beta1 (TGF-beta1) has an important role in the pathogenesis of glomerular damage by influencing matrix metabolism. An association of TGF-beta1 with glomerulosclerosis and interstitial fibrosis has been shown in various renal diseases, suggesting that TGF-beta1 may serve as a diagnostic marker of glomerular diseases. The aim of this study is to determine the usefulness of urinary TGF-beta1 values to monitor therapeutic effects of steroids in patients with immunoglobulin A (IgA) nephropathy. Concentrations and activation rates of TGF-beta1 (mature/total) were determined in urine of patients with renal diseases by means of a double-antibody enzyme immunoassay. The urinary TGF-beta1 level before steroid therapy was compared with renal histological characteristics, creatinine clearance, and proteinuria in patients with a variety of renal diseases. Urinary excretion of total and mature TGF-beta1 was significantly greater in patients with crescentic glomerulonephritis and IgA nephropathy than in healthy controls, whereas the activation rate of urinary TGF-beta1 was similar among patients with other renal diseases. Urinary TGF-beta1 excretion at the time of renal biopsy significantly correlated with the degree of crescent formation in patients with IgA nephropathy, but not in those with glomerular sclerosis or tubulointerstitial fibrosis. Urinary excretion of total and mature TGF-beta1 was reduced in patients with IgA nephropathy after treatment with prednisolone (0.8 mg/kg/d) for 1 month. The activation rate of urinary TGF-beta1 also decreased significantly after steroid therapy. Urinary TGF-beta1 values therefore may be useful to assess disease activity or the effects of steroid therapy in patients with IgA nephropathy.
authors.affiliation: Departments of Nephrology and Internal Medicine III, Kurume University School of Medicine, Kurume, Japan. haramaki@med.kurume-u.ac.jp
authors.forename: R
authors.initials: R
authors.lastname: Haramaki
authors.forename: K
authors.initials: K
authors.lastname: Tamaki
authors.forename: M
authors.initials: M
authors.lastname: Fujisawa
authors.forename: H
authors.initials: H
authors.lastname: Ikedo
authors.forename: N
authors.initials: N
authors.lastname: Haramaki
authors.forename: S
authors.initials: S
authors.lastname: Okuda
mesh_terms: D000293:Adolescent; D000328:Adult; D004109:Dilazep / Q000627:therapeutic use*; D005260:Female; D005921:Glomerulonephritis / Q000652:urine; D005922:Glomerulonephritis, IGA / Q000097:blood / Q000188:drug therapy* / Q000473:pathology / Q000652:urine*; D006801:Humans; D007150:Immunohistochemistry; D007668:Kidney / Q000473:pathology; D008297:Male; D008875:Middle Aged; D008991:Monitoring, Physiologic; D011239:Prednisolone / Q000627:therapeutic use*; D016212:Transforming Growth Factor beta / Q000097:blood / Q000652:urine*; D053773:Transforming Growth Factor beta1
chemical_list: C508960:TGFB1 protein, human; D016212:Transforming Growth Factor beta; D053773:Transforming Growth Factor beta1; D011239:Prednisolone; D004109:Dilazep