title: Relevance of periglomerular myofibroblasts in progression of human glomerulonephritis.
abstract: To clarify the pathological and clinical significance of periglomerular alpha-smooth muscle actin (alpha-SMA)-positive cells, we examined 51 needle-biopsy specimens from patients with human glomerulonephritis. Immunoelectron microscopy confirmed these cells were myofibroblasts showing characteristic features with abundant alpha-SMA-positive thin myofilaments. Nonsclerotic glomeruli with periglomerular myofibroblasts were larger in the Bowman's capsular planar area than nonsclerotic glomeruli without periglomerular myofibroblasts (24.7 +/- 6.0 x 10(3) microm2 v 19.9 +/- 8.5 x 10(3) microm2; P < 0.01). We studied the correlation between the clinical prognosis and the extent of periglomerular myofibroblasts in 24 patients with IgA nephropathy. Patients were divided into two groups; those with plasma creatinine levels within normal range at biopsy and significantly elevated at follow-up were designated group 1 (poor prognosis), and patients with plasma creatinine levels within normal range at biopsy and not significantly elevated at follow-up were designated group 2 (fair prognosis). In the kidneys of group 1 patients, periglomerular alpha-SMA was expressed more intensively than it was in the kidneys of group 2 patients (alpha-SMA expression score, 1.0 +/- 0.48 v 0.52 +/- 0.54; P < 0.05). These findings indicate that periglomerular myofibroblasts appeared surrounding the nonsclerotic hypertrophic glomeruli, which may lead finally to glomerulosclerosis. This report suggests that interaction between the glomerular cells and the periglomerular myofibroblasts may have a role in the progression of glomerular diseases.
authors.affiliation: The Second Department of Internal Medicine, Faculty of Medicine, the University of Tokyo, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Oba
authors.forename: K
authors.initials: K
authors.lastname: Kimura
authors.forename: N
authors.initials: N
authors.lastname: Suzuki
authors.forename: N
authors.initials: N
authors.lastname: Mise
authors.forename: A
authors.initials: A
authors.lastname: Tojo
authors.forename: K
authors.initials: K
authors.lastname: Miyashita
authors.forename: Y
authors.initials: Y
authors.lastname: Konno
authors.forename: Y
authors.initials: Y
authors.lastname: Hirata
authors.forename: A
authors.initials: A
authors.lastname: Goto
authors.forename: M
authors.initials: M
authors.lastname: Omata
mesh_terms: D008841:Actin Cytoskeleton / Q000473:pathology; D000199:Actins / Q000378:metabolism*; D000293:Adolescent; D000328:Adult; D001707:Biopsy, Needle; D003404:Creatinine / Q000097:blood; D005260:Female; D005347:Fibroblasts / Q000473:pathology; D005921:Glomerulonephritis / Q000473:pathology*; D005922:Glomerulonephritis, IGA / Q000473:pathology; D005923:Glomerulosclerosis, Focal Segmental / Q000473:pathology; D006801:Humans; D006984:Hypertrophy; D007124:Immunoenzyme Techniques; D007678:Kidney Glomerulus / Q000473:pathology; D008297:Male; D008875:Middle Aged; D011379:Prognosis
chemical_list: D000199:Actins; D003404:Creatinine