title: Significance of glomerular cell apoptosis in the resolution of acute post-streptococcal glomerulonephritis.
abstract: BACKGROUND
  Glomerular hypercellularity due to resident glomerular cell proliferation and leucocyte infiltration has been described in acute post-streptococcal glomerulonephritis (APSGN). APSGN usually resolves without progression. However, the mechanism of resolution remains to be determined.
  
  
  METHODS
  Renal biopsy tissues from 15 patients with APSGN (obtained 1-31 days after disease onset) and five control patients with minor glomerular abnormality were evaluated with respect to glomerular resolution. Apoptotic cells were assessed by terminal deoxynucleotidyl transferase-mediated dUTP nick end-labelling (TUNEL) as well as by immunostaining of single-stranded DNA (ssDNA).
  
  
  RESULTS
  The number of glomerular cells was high in the early-phase of APSGN and decreased over time. No TUNEL+ glomerular cells were found in control subjects, whereas prominent glomerular TUNEL+ cells were observed in APSGN patients, particularly in the early phase of the disease. The number of glomerular TUNEL+ cells decreased exponentially but was still prominent in renal tissue biopsied at 31 days after disease onset. Double staining for ssDNA and glomerular cell markers showed that glomerular apoptotic cells were predominantly mesangium and endothelial cells, with some neutrophils and macrophages.
  
  
  CONCLUSIONS
  These results suggest that apoptosis exists in the glomerulus in patients with APSGN from the early to the late stages of the disease and contributes to the resolution of glomerular hypercellularity.
authors.affiliation: Department of Medicine, National Defense Medical College, 3-2 Namiki, Tokorozawa-shi, Saitama 359-8513, Japan. takashio@ndmc.ac.jp
authors.forename: Takashi
authors.initials: T
authors.lastname: Oda
authors.forename: Nobuyuki
authors.initials: N
authors.lastname: Yoshizawa
authors.forename: Kazuo
authors.initials: K
authors.lastname: Yamakami
authors.forename: Aki
authors.initials: A
authors.lastname: Ishida
authors.forename: Osamu
authors.initials: O
authors.lastname: Hotta
authors.forename: Shigenobu
authors.initials: S
authors.lastname: Suzuki
authors.forename: Soichiro
authors.initials: S
authors.lastname: Miura
mesh_terms: D000208:Acute Disease; D000293:Adolescent; D000328:Adult; D000942:Antigens, Bacterial / Q000235:genetics / Q000378:metabolism; D015703:Antigens, CD / Q000276:immunology; D015214:Antigens, Differentiation, Myelomonocytic / Q000276:immunology; D017209:Apoptosis; D015415:Biomarkers / Q000378:metabolism; D049109:Cell Proliferation; D002648:Child; D004277:DNA, Single-Stranded / Q000032:analysis; D018450:Disease Progression; D005260:Female; D005341:Fibrinolysin / Q000378:metabolism; D005921:Glomerulonephritis / Q000209:etiology / Q000378:metabolism / Q000473:pathology*; D006801:Humans; D020287:In Situ Nick-End Labeling; D007678:Kidney Glomerulus / Q000378:metabolism / Q000473:pathology*; D008264:Macrophages / Q000276:immunology; D008297:Male; D008875:Middle Aged; D011956:Receptors, Cell Surface / Q000235:genetics / Q000378:metabolism; D013290:Streptococcal Infections / Q000150:complications* / Q000378:metabolism / Q000382:microbiology / Q000473:pathology; D000097382:CD68 Molecule
chemical_list: D000942:Antigens, Bacterial; D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D015415:Biomarkers; D004277:DNA, Single-Stranded; D005341:Fibrinolysin; D011956:Receptors, Cell Surface; C067980:CD68 antigen, human; D000097382:CD68 Molecule; C517776:nephritis-associated plasminogen receptor, Streptococcus