Renal expression of alpha-smooth muscle actin and c-Met in children with Henoch-Schönlein purpura nephritis.
Alpha-smooth muscle actin (alpha-SMA) is the actin isoform that predominates within vascular smooth-muscle cells and plays an important role in fibrogenesis. On the other hand, c-Met is the receptor for hepatocyte growth factor (HGF), which plays a role in protection from injury and has anti-fibrogenetic effects. To clarify whether alpha-SMA and HGF are associated with the progression of renal injury in Henoch-Schönlein purpura nephritis (HSPN), we evaluated the renal expression of alpha-SMA and c-Met in HSPN patients. Patients were divided into three groups. Group 1 consisted of eight patients (male:female 4:4) with stage II or less in the classification of the International Study of Kidney Disease in Children (ISKDC), Group 2 consisted of 20 patients (male:female 11:9) with ISKDC stage III or greater and a good prognosis, and group 3 consisted of seven patients (male:female 3:4) with ISKDC stage III or greater and poor prognosis. Renal biopsy findings, including c-Met and alpha-SMA staining, were investigated for each group. At first biopsy, the mean scores for renal alpha-SMA and glomerular c-Met in groups 2 and 3 were higher than those in group 1, while mean scores for neither renal alpha-SMA nor glomerular c-Met differed between groups 2 and 3. At second biopsy, the mean scores for renal alpha-SMA staining in group 3 were higher than those in group 2, and mean score for glomerular c-Met staining in group 3 was lower than that in group 2. In groups 2 and 3, the mean scores for glomerular and interstitial alpha-SMA staining at first biopsy were correlated with the chronicity index (CI) at second biopsy, but the mean score for glomerular c-Met staining at first biopsy correlated with neither the activity index (AI) nor CI in the first or second biopsies in all groups. Our findings suggest that the expression of renal alpha-SMA may be associated with progression of renal injury in HSPN.
Kawasaki
Yukihiko
Y
Department of Pediatrics, Fukushima Medical University School of Medicine, 1 Hikariga-oka, Fukushima City, Fukushima 960-1295, Japan. tomo@fmu.ac.jp
Imaizumi
Tomoko
T
Matsuura
Hiromi
H
Ohara
Shinichirou
S
Takano
Kei
K
Suyama
Kazuhide
K
Hashimoto
Koichi
K
Nozawa
Ruriko
R
Suzuki
Hitoshi
H
Hosoya
Mitsuaki
M
D000199:Actins / Q000032:analysis*; D001706:Biopsy; D002648:Child; D018450:Disease Progression; D005260:Female; D006801:Humans; D011695:IgA Vasculitis / Q000150:complications* / Q000378:metabolism / Q000473:pathology; D007678:Kidney Glomerulus / Q000737:chemistry* / Q000473:pathology; D008297:Male; D009393:Nephritis / Q000209:etiology / Q000378:metabolism* / Q000473:pathology; D011379:Prognosis; D019859:Proto-Oncogene Proteins c-met / Q000032:analysis*; D012189:Retrospective Studies; D012720:Severity of Illness Index
D000199:Actins; D019859:Proto-Oncogene Proteins c-met