Pediatr Nephrol (2008) 23:1257–1267 findings, and urinary findings (proteinuria and hematuria) in patients with MGA or IgAN (Fig. 6). The glomerular AGT expression was positively correlated with ang II (r = +0.711, P < 0.001) (Fig. 6a), TGF-β (r = +0.723, P < 0.001) (Fig. 6b), α-SM actin (r = +0.565, P < 0.005) (Fig. 6c), glomerular cell number (r = +0.542, P < 0.005) (Fig. 6d), GS score (r = +0.768, P < 0.001) (Fig. 6e), and proteinuria (r = +0.436, P < 0.05) (Fig. 6f). Similarly, glomerular ang II level showed a significant positive correlation with that of TGF-β (r = +0.782, P < 0.001) (Fig. 6g), α-SM actin (r = +0.640, P < 0.001) (Fig. 6h), cell number (r = +0.441, P < 0.05) (Fig. 6i), GS score (r = 0.826, P < 0.001) (Fig. 6j), and proteinuria (r = +0.364, P < 0.05) (Fig. 6k). However, neither AGT nor ang II showed a significant correlation with expression of ACE, AT1R, and hematuria index. Finally, a positive correlation was demonstrated between TGF-β and α-SM actin (r = +0.625, P < 0.001) (Fig. 6l). 1263 Effect of ang II on the AGT mRNA and protein levels by human GEC The regulation of AGT expression by GEC and a possible role of GEC-AGT in disease progression of IgAN were examined using cultured human GEC. The addition of 10−7 M ang II rapidly induced AGT mRNA expression of quiescent human GEC after stimulation for 1 h. This increase peaked at 3 h, with a sevenfold increase, and then gradually decreased during the course of the experiment (Fig. 7a). When the response of AGT transcript to ang II dose was investigated after incubation for 3 h, a dose- dependent increase between 10−11 and 10−7 M was seen (Fig. 7b). Western blot analysis revealed a time-dependent increase of AGT protein product to 10−7 M ang II stimulation. The increased expression of AGT protein followed the increase of AGT mRNA by GEC and peaked Fig. 6 Plots of correlations between the staining levels of angio- tensinogen (AGT) and angiotensin II (ang II) (a), AGT and transforming growth factor-β (TGF-β) (b), AGT and α-smooth-muscle (α-SM) actin (c), AGT and glomerular cell number (cell number) (d), AGT and glomerulosclerosis (GS) score (e), AGT and proteinuria (f), ang II and TGF-β (g), ang II and α-SM actin (h), ang II and cell number (i), ang II and GS score (j), ang II and proteinuria (k), and TGF-β and α-SM actin (l) in patients with minor glomerular abnormalities (MGA) (○) or immunoglobulin A nephropathy (IgAN) (•) (correlation; P value) The levels of AGT positively correlate with the level of ang II (r=+0.711; P<0.001), TGF-β (r=+0.723; P<0.001), cell number (r=+0.542; P< 0.005), GS score (r=+0.768; P<0.001), and proteinuria (r=+0.436; P<0.05). Ang II is also positively correlated with TGF-β (r=+0.782; P<0.001), α-SM actin (r=+0.640; P<0.001), cell number (r=+ 0.441; P<0.05), GS score (r=+0.826; P<0.001), and proteinuria (r= +0.364; P<0.05). The levels of TGF-β positively correlate with the level of α-SM actin (r=+0.625; P<0.001)