title: Activation of the lectin complement pathway in Henoch-Schönlein purpura nephritis.
abstract: BACKGROUND
  We previously reported the existence of complement activation through the alternative and lectin pathways in patients with immunoglobulin A (IgA) glomerulonephritis (GN). The current study aims to elucidate the correlation between each complement pathway and clinicopathologic findings in patients with Henoch-Schonlein purpura nephritis (HSPN).
  
  
  METHODS
  Immunohistologic staining was performed on renal specimens obtained from 31 patients with HSPN and 20 controls as non-IgA GN by using antibodies against IgG, IgA, IgA1, IgA2, IgM, C1q, C3c, C4, fibrinogen, factor B, C4-binding protein (C4-bp), C5b-9, CD59, mannose-binding lectin (MBL), and MBL-associated serine protease-1 (MASP-1).
  
  
  RESULTS
  No control showed deposition of any antibody. In 16 patients with mesangial IgA1/IgA2 codeposits, mesangial deposits of C3c, C4, factor B, C4-bp, C5b-9, CD59, MBL, and MASP-1 were found. In the remaining 15 patients with mesangial IgA1 deposits alone, no mesangial deposits of C4 or MBL/MASP-1 were found, and mesangial deposits of C3c, factor B, C5b-9, and CD59 were evident in 11 patients. Glomerular deposits of fibrinogen were detected in 15 of 16 patients with IgA1/IgA2 codeposits and only 6 of 15 patients with IgA1 deposits. Severity of glomerular changes and degrees of hematuria and proteinuria at latest follow-up were greater in patients with IgA1/IgA2 codeposits than in those with IgA1 deposits.
  
  
  CONCLUSIONS
  Complement activation through both the alternative and lectin pathways is found in patients with HSPN. Complement activation is promoted in situ in the glomerulus. MBL/MASP-1 may be associated with glomerular deposition of fibrinogen. Complement activation through the lectin pathway may contribute to the development of advanced glomerular injuries and prolonged urinary abnormalities in patients with HSPN.
authors.affiliation: Department of Pathology, School of Medicine, Fukuoka University, Fukuoka, Japan. hisan@cis.fukuoka-u.ac.jp <hisan@cis.fukuoka-u.ac.jp>
authors.forename: Satoshi
authors.initials: S
authors.lastname: Hisano
authors.forename: Misao
authors.initials: M
authors.lastname: Matsushita
authors.forename: Teizo
authors.initials: T
authors.lastname: Fujita
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Iwasaki
mesh_terms: D000293:Adolescent; D001706:Biopsy; D002648:Child; D002675:Child, Preschool; D003167:Complement Activation / Q000502:physiology*; D037582:Complement Pathway, Mannose-Binding Lectin / Q000502:physiology*; D016650:Fluorescein-5-isothiocyanate / Q000031:analogs & derivatives / Q000378:metabolism; D005920:Glomerular Mesangium / Q000737:chemistry / Q000378:metabolism / Q000473:pathology; D005922:Glomerulonephritis, IGA / Q000235:genetics / Q000473:pathology; D006801:Humans; D011695:IgA Vasculitis / Q000235:genetics / Q000473:pathology*; D007070:Immunoglobulin A / Q000276:immunology; D007150:Immunohistochemistry / Q000379:methods; D007668:Kidney / Q000737:chemistry / Q000473:pathology; D010641:Phenotype; D012710:Serum Albumin, Bovine / Q000378:metabolism
chemical_list: D007070:Immunoglobulin A; C039217:fluorescein isothiocyanate bovine serum albumin; D012710:Serum Albumin, Bovine; D016650:Fluorescein-5-isothiocyanate