title: Characterization and quantification of proliferating cell patterns in endocapillary proliferation.
abstract: BACKGROUND
  Endocapillary proliferation (EP) is a common pathological finding in proliferative glomerulonephritis (GN). Its appearance indicates the presence of active lesions of GN. In this study, we reinvestigated the pathological features of EP.
  
  
  METHODS
  Cell markers that included CD15, CD68, CD45RO, CD31 and alpha-smooth muscle actin (alpha-SMA) were used to identify the intraglomerular cells in renal biopsy tissues collected from patients with post-streptococcal acute GN (PSAGN), methicillin-resistant Staphylococcus aureus-associated GN (MRSAGN) with or without EP, membranoproliferative GN (MPGN) with or without EP, Henoch-Schönlein nephritis, immunoglobulin A nephropathy, membranous nephropathy and minimal change nephrotic syndrome. Proliferating cells and apoptotic cells were investigated simultaneously.
  
  
  RESULTS
  The glomerular infiltrating polymorphonuclear leukocytes, macrophages, T cells, mesangial cells and endothelial cells were enumerated. In PSAGN, the glomerulus was enlarged and all cell types were greatly increased. In MRSAGN EP, the glomerulus was slightly enlarged with abundant infiltrating leukocytes and monocyte/macrophages and had moderate mesangial cell proliferation with negligible endothelial cell proliferation. In MPGN, the glomerulus markedly enlarged with multiple monocyte/macrophages and remarkable mesangial proliferation. The mesangial cells in EP glomeruli were highly activated as evidenced by alpha-SMA expression, particularly in PSAGN.
  
  
  CONCLUSIONS
  This is the first report to use monoclonal antibodies specific for cell markers to quantitatively analyze and compare the proliferating cell types in EP glomeruli in different forms of GN. The results suggest that identification of the presence of polymorphonuclear leukocytes in the capillary lumen might help in differentiating between glomerular global and segmental EP.
authors.affiliation: Department of Internal Medicine, Tokai University School of Medicine, Isehara, Kanagawa, Japan. qwu2003@is.icc.u-tokai.ac.jp
authors.forename: Qiong
authors.initials: Q
authors.lastname: Wu
authors.forename: Hisae
authors.initials: H
authors.lastname: Tanaka
authors.forename: Takashi
authors.initials: T
authors.lastname: Hirukawa
authors.forename: Masayuki
authors.initials: M
authors.lastname: Endoh
authors.forename: Masafumi
authors.initials: M
authors.lastname: Fukagawa
mesh_terms: D000199:Actins / Q000378:metabolism; D000911:Antibodies, Monoclonal; D015703:Antigens, CD / Q000378:metabolism; D015214:Antigens, Differentiation, Myelomonocytic / Q000378:metabolism; D017209:Apoptosis; D015415:Biomarkers / Q000378:metabolism; D002196:Capillaries / Q000378:metabolism / Q000473:pathology; D049109:Cell Proliferation; D005260:Female; D005647:Fucosyltransferases / Q000378:metabolism; D005921:Glomerulonephritis / Q000145:classification / Q000378:metabolism / Q000473:pathology*; D005922:Glomerulonephritis, IGA / Q000378:metabolism / Q000473:pathology; D015432:Glomerulonephritis, Membranoproliferative / Q000378:metabolism / Q000473:pathology; D006801:Humans; D011695:IgA Vasculitis / Q000378:metabolism / Q000473:pathology; D007150:Immunohistochemistry; D007678:Kidney Glomerulus / Q000098:blood supply / Q000378:metabolism / Q000473:pathology; D017493:Leukocyte Common Antigens / Q000378:metabolism; D016256:Lewis X Antigen / Q000378:metabolism; D008297:Male; D009402:Nephrosis, Lipoid / Q000378:metabolism / Q000473:pathology; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000378:metabolism; D000097382:CD68 Molecule
chemical_list: D000199:Actins; D000911:Antibodies, Monoclonal; D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D015415:Biomarkers; D005647:Fucosyltransferases; D017493:Leukocyte Common Antigens; D016256:Lewis X Antigen; D019408:Platelet Endothelial Cell Adhesion Molecule-1; C541116:ACTA2 protein, human; C067980:CD68 antigen, human; D000097382:CD68 Molecule; C066693:FUT4 protein, human