title: [Clinicopathologic analysis of 34 patients with microscopic polyangitis].
abstract: OBJECTIVE
  To study the clinicopathologic features of microscopic polyangitis (MPA), and to compare the differences in anti-neutrophil cytoplasmic autoantibody (ANCA)-positive and ANCA-negative patients, as well as in ANCA-positive cases with or without glomerular immunoglobulin deposition.
  
  
  METHODS
  Thirty-four biopsy-proven cases of MPA were retrieved from the archival files of the Department during the past 7 years. The clinicopathologic characteristics between ANCA-positive and negative patients, as well as between ANCA-positive cases with and without glomerular immunoglobulin deposition, were compared.
  
  
  RESULTS
  Amongst the 34 MPA patients studied, about one-fifth to one-half were accompanied by various extrarenal symptoms. Serum ANCA was positive in 26 patients (76.5%). A slight to moderate increase in urinary protein was demonstrated in 31 patients, while 3 patients had nephrotic syndrome. Elevated serum creatinine was detected in 32 cases. Renal biopsy revealed crescentic glomerulonephritis in 24 cases, focal segmental glomerulonephritis in 8 cases, vascular fibrinoid necrosis with inflammation in 7 cases, intimal thickening of arterioles in 24 cases, interstitial inflammatory cells, including neutrophil infiltration (21 cases), in 29 cases. Crescentic formation was more common in the ANCA-positive group than in the ANCA-negative group (P < 0.05). Amongst the 26 ANCA-positive cases, 10 had glomerular immunoglobulin deposits (including 1 case with IgA nephropathy). In general, these cases had a greater degree of proteinuria than those without glomerular immunoglobulin deposits (P < 0.05).
  
  
  CONCLUSIONS
  The diagnosis of MPA relies on histologic examination of renal biopsy and clinicopathologic correlation. Serum ANCA seems important for glomerular crescent formation. Glomerular immunoglobulin deposition may also play a significant role in the exacerbation of proteinuria.
authors.affiliation: Department of Pathology, Shanghai Medical College, Fudan University, Shanghai 200032, China.
authors.forename: Xian-fa
authors.initials: XF
authors.lastname: Xuan
authors.forename: Hui-juan
authors.initials: HJ
authors.lastname: Wu
authors.forename: Ye
authors.initials: Y
authors.lastname: Liu
authors.forename: Zhong-hua
authors.initials: ZH
authors.lastname: Zhao
authors.forename: Feng-ying
authors.initials: FY
authors.lastname: Hong
authors.forename: Yu-xin
authors.initials: YX
authors.lastname: Wang
authors.forename: Zhi-gang
authors.initials: ZG
authors.lastname: Zhang
authors.forename: Mu-yi
authors.initials: MY
authors.lastname: Guo
mesh_terms: D000328:Adult; D000368:Aged; D019268:Antibodies, Antineutrophil Cytoplasmic / Q000378:metabolism*; D015415:Biomarkers; D001706:Biopsy; D005260:Female; D005921:Glomerulonephritis / Q000378:metabolism / Q000473:pathology; D006801:Humans; D007132:Immunoglobulin Isotypes / Q000378:metabolism; D007668:Kidney / Q000473:pathology*; D007674:Kidney Diseases / Q000378:metabolism / Q000473:pathology*; D008297:Male; D008875:Middle Aged; D009404:Nephrotic Syndrome / Q000378:metabolism / Q000473:pathology; D011507:Proteinuria / Q000473:pathology; D012189:Retrospective Studies; D014657:Vasculitis / Q000378:metabolism / Q000473:pathology*
chemical_list: D019268:Antibodies, Antineutrophil Cytoplasmic; D015415:Biomarkers; D007132:Immunoglobulin Isotypes