title: Discrepancies in glomerular and tubulointerstitial/vascular immune complex IgG subclasses in lupus nephritis.
abstract: OBJECTIVE
  Lupus nephritis is characterized by glomerular and extraglomerular immune complex deposition in the kidney. It is unclear whether the same circulating immune complexes deposit in the glomeruli and in extraglomerular structures, or whether they are pathogenetically different. Differences in the IgG subclass composition may point towards different pathways in the formation of glomerular and extraglomerular immune complexes. Therefore we investigated IgG subclass distribution in the immune complex deposits at these anatomic sites.
  
  
  METHODS
  A total of 84 biopsies diagnosed as lupus nephritis and classified according to the International Society of Nephrology/Renal Pathology Society (ISN/RPS) 2003 classification, were examined by direct immunofluorescence staining for IgG subclasses. The IgG subclass composition in the glomerular, tubular basement membrane (TBM) and vascular wall deposits was compared. We also correlated the presence/absence of interstitial inflammation and IgG subclasses in the TBM and vascular deposits. Lastly, we looked for correlation between staining for IgG subclasses and complement C1q and C3 staining.
  
  
  RESULTS
  IgG staining was present in the TBM in 52/84 biopsies, and in the vascular walls in 40/84 biopsies. IgG subclass distribution was discrepant between glomerular and TBM deposits in 36/52 biopsies, and between glomerular and vascular deposits in 27/40 biopsies. Interstitial inflammation did not correlate with the presence of IgG staining or distribution of IgG subclasses in the TBM. Interstitial inflammation was more common in biopsies of African-American patients than Caucasian patients. The IgG subclass staining correlated with C1q staining in all the three compartments.
  
  
  CONCLUSIONS
  The antibody composition of the glomerular and extraglomerular immune complex deposits appear to differ from each other. They may not represent the same preformed immune complexes from the circulation. It is likely that their pathogenesis and site of formation are different.
authors.affiliation: Department of Pathology, The Ohio State University Medical Center, M018 Starling Loving Hall, 320 W 10th Ave, Columbus, OH 43210, USA. anjali.satoskar@osumc.edu
authors.forename: A A
authors.initials: AA
authors.lastname: Satoskar
authors.forename: S V
authors.initials: SV
authors.lastname: Brodsky
authors.forename: G
authors.initials: G
authors.lastname: Nadasdy
authors.forename: C
authors.initials: C
authors.lastname: Bott
authors.forename: B
authors.initials: B
authors.lastname: Rovin
authors.forename: L
authors.initials: L
authors.lastname: Hebert
authors.forename: T
authors.initials: T
authors.lastname: Nadasdy
mesh_terms: D000328:Adult; D000368:Aged; D000936:Antigen-Antibody Complex / Q000276:immunology*; D001706:Biopsy; D015922:Complement C1q / Q000276:immunology; D003176:Complement C3 / Q000276:immunology; D005260:Female; D006801:Humans; D007074:Immunoglobulin G / Q000276:immunology*; D007678:Kidney Glomerulus / Q000276:immunology* / Q000473:pathology; D007684:Kidney Tubules / Q000276:immunology* / Q000473:pathology; D008181:Lupus Nephritis / Q000276:immunology* / Q000473:pathology; D008297:Male; D008875:Middle Aged; D055815:Young Adult
chemical_list: D000936:Antigen-Antibody Complex; D003176:Complement C3; D007074:Immunoglobulin G; D015922:Complement C1q