title: Long-term renal injury in ANCA-associated vasculitis: an analysis of 31 patients with follow-up biopsies.
abstract: BACKGROUND
  We reported previously that in renal disease in relation to antineutrophil cytoplasm auto-antibodies (ANCA)-associated vasculitis, renal outcome correlates better with the percentage of normal glomeruli than with separate active lesions. This may imply that glomeruli, once affected by necrotizing and crescentic lesions, are irreversibly damaged. We quantified and evaluated the course of renal lesions in the present study.
  
  
  METHODS
  We retrospectively analysed 31 patients with renal disease in relation to ANCA-associated vasculitis, all treated with immunosuppressive drugs. In all patients, a renal biopsy was performed at diagnosis. A follow-up biopsy was performed in all patients on the indication of a suspected renal relapse, after a mean interval of 31 months.
  
  
  RESULTS
  The mean percentage of normal glomeruli in the renal biopsy did not change over time (29% in the initial and 30% in the follow-up biopsy). The mean percentage of glomeruli with crescents, however, significantly decreased from 57 to 30% (P<0.001). The percentage of glomerulosclerosis significantly increased from 12 to 39% (P<0.001). The data were independent of diagnosis, gender, age, time interval between the biopsies, and treatment.
  
  
  CONCLUSIONS
  This is the first study to quantify glomerular changes between two time points in patients with renal vasculitis. Our results suggest that, on average, no new glomeruli are recruited into the active disease process. The sum of the percentage of crescentic and sclerotic glomeruli in the initial biopsies is larger than the percentage of sclerotic glomeruli in the follow-up biopsies. Thus, therapy seems not only to prevent normal glomeruli from being recruited into the active disease process for a certain time, but seems also to allow part of the active lesions to revert into a normal phenotype, although another part of the active lesions will be transformed to a chronic phenotype.
authors.affiliation: Department of Pathology, Leiden University Medical Center, Leiden, The Netherlands. H.A.Hauer@LUMC.nl
authors.forename: Herbert A
authors.initials: HA
authors.lastname: Hauer
authors.forename: Ingeborg M
authors.initials: IM
authors.lastname: Bajema
authors.forename: E Christiaan
authors.initials: EC
authors.lastname: Hagen
authors.forename: Laure-Hélène
authors.initials: LH
authors.lastname: Noël
authors.forename: Franco
authors.initials: F
authors.lastname: Ferrario
authors.forename: Rüdiger
authors.initials: R
authors.lastname: Waldherr
authors.forename: Hans C
authors.initials: HC
authors.lastname: van Houwelingen
authors.forename: Philippe
authors.initials: P
authors.lastname: Lesavre
authors.forename: Renato A
authors.initials: RA
authors.lastname: Sinico
authors.forename: Fokko
authors.initials: F
authors.lastname: van der Woude
authors.forename: Gill
authors.initials: G
authors.lastname: Gaskin
authors.forename: Cornelis A
authors.initials: CA
authors.lastname: Verburgh
authors.forename: Emile
authors.initials: E
authors.lastname: de Heer
authors.forename: Jan A
authors.initials: JA
authors.lastname: Bruijn
mesh_terms: D000328:Adult; D000368:Aged; D019268:Antibodies, Antineutrophil Cytoplasmic / Q000032:analysis*; D001706:Biopsy; D002455:Cell Division; D003404:Creatinine / Q000097:blood; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D007668:Kidney / Q000473:pathology*; D008297:Male; D008875:Middle Aged; D009336:Necrosis; D012189:Retrospective Studies; D014657:Vasculitis / Q000473:pathology*
chemical_list: D019268:Antibodies, Antineutrophil Cytoplasmic; D003404:Creatinine