Urinary Transforming Growth Factor-beta-inducible Gene-h3 in Patients with Glomerular Diseases.
- Author:
Hee Joo HONG
1
;
Sung Do KIM
;
Byoung Cheol LEE
;
Hee Jung YOON
;
Eun Hee BAE
;
Byoung Soo CHO
Author Information
1. Department of Pediatrics, Gil Medical Center, Gachon Medical Center, Incheon, Korea.
- Publication Type:Original Article
- MeSH:
Enzyme-Linked Immunosorbent Assay;
Female;
Glomerulonephritis;
Glomerulonephritis, Membranoproliferative;
Humans;
Kidney Diseases;
Male;
Nephrosis, Lipoid;
Nephrotic Syndrome;
Seoul;
Transforming Growth Factor alpha
- From:Korean Journal of Nephrology
2006;25(2):229-234
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGOUND: Transforming growth factor-beta (TGF-alpha) has been implicated in the pathogenesis of a number of kidney diseases. However, TGF-alpha is secreted in a latent form requiring extracellular modification to become biologically active. Recently, the activity of TGF-alpha has been assessed by the measurement betaig-h3, a novel TGF-alpha induced gene product. Thus we evaluated the pattern of urinary betaig-h3 expression in various glomerular diseases. METHODS: 64 patients with biopsy-proven primary glomerulonephritis (FSGS 6, HSPN 16, IgAN 20, MPGN I 7, and MesPGN 15), 10 patients with nephrotic syndrome and 12 healthy controls were enrolled in the study. A total 86 subjects (51 males, 59.3% and 35 females, 40.7%, mean age 13.9+/-4.28 years) constituted study population. First morning urine were collected and betaig-h3 in the urine was determined by indirect competitive ELISA (Regen Biotech Inc, Seoul, Korea). RESULTS: betaig-h3 excretion was significantly higher in the urine from patients with HSPN (27.5+/-6.46, p=0.002), with IgAN (40.83+/-12.27, p=0.026), with MPGN I (21.64+/-7.29, p=0.042), MesPGN (26.42+/-6.68, p=0.007). In patients with FSGS (21.65+/-17.12) and minimal change nephrotic syndrome (6.26+/-2.18), mean urinary betaig-h3 excretion was not significant higher than that in control group (3.56+/-0.78). CONCLUSION: Urinary betaig-h3 excretion was high in proliferative renal diseases. However, betaig-h3 excretion was not high in non-proliferative renal diseases.
