K. Takazoe et al., Urinary transforming growth factor-beta 1 is an indicator of histological chronicity in IgA nephropathy, NEPHROLOGY, 5(4), 2000, pp. 231-236
This study examined urinary excretion of transforming growth factor-beta1 (
TGF-beta1) in adult IgA nephropathy and compared this with clinical and his
tological parameters. TGF-beta1 was measured by enzyme-linked immunosorbent
assay in 24-h urine specimens from 25 patients with IgA nephropathy (17 me
n, eight women). Urine from eight age-matched control subjects served as th
e control. Serum TGF-beta1 was also measured in 16 out of the 25 patients a
nd six age-matched control subjects. TGF-beta1 was detected in the urine in
72% of IgA nephropathy patients(18/25), but was not detected in any of the
control subjects. Patients with decreased renal function (creatinine clear
ance (Ccr) < 80 mL/min) had higher urine levels of TGF-beta1 than those wit
h normal renal function (Ccr greater than or equal to 80 mL/min) (141.8 +/-
60.0 ng/day vs 39.7 +/- 33.2 ng/day, P < 0.01). The level of TGF-beta1 gav
e a negative correlation with Ccr (r = -0.62, P = 0.001), but not with prot
einuria (r = 0.11, P = 0.58). Twenty-two of the patients were evaluated his
tologically. The urinary TGF-beta1 levels correlated with both global scler
osis and interstitial volume (r = 0.52, P < 0.05, and r = 0.51, P < 0.05, r
espectively). However, there was no correlation between TGF-beta1 levels an
d glomerular intracapillary inflammatory cell score, mesangial proliferatio
n score or the matrix score. No correlation was found between TGF-beta1 lev
els and the number of glomerular or interstitial CD68(+) cells. No signific
ant differences in serum TGF-beta1 levels were observed between patients wi
th normal Ccr and those with decreased Ccr. Also, its levels were found to
be independent of the urine levels. In conclusion, 24-h urinary TGF-beta1 e
xcretion was found to correlate with Ccr, global sclerosis and interstitial
volume, demonstrating that urinary TGF-beta1 is an indicator of chronicity
in adult IgA nephropathy.