title: Anti-centromere antibody is an independent risk factor for chronic kidney disease in patients with primary biliary cirrhosis.
abstract: BACKGROUND
  Anti-centromere antibody (ACA), a typical autoantibody of systemic sclerosis, is also detected in primary biliary cirrhosis (PBC). However, its pathogenic role is not fully understood. The aim of this study was to determine the association between ACA and kidney function in PBC.
  
  
  METHODS
  A cohort of 37 patients diagnosed as having PBC from July 2001 to November 2011 at Yokosuka Kyosai Hospital was retrospectively analyzed for a follow-up period of 12 months. The annual rate of estimated glomerular filtration rate (eGFR) decline within 1 year after the diagnosis was evaluated. The factors associated with eGFR decline were evaluated by linear regression analysis and logistic regression analysis.
  
  
  RESULTS
  Overall, 37 PBC patients were included, of whom 12 (32%) had ACA. The patients with ACA had a lower eGFR (65.9 ± 19.9 vs. 80.3 ± 12.1 mL/min/1.73 m(2), P = 0.01), a higher likelihood of chronic kidney disease (CKD) (58 vs. 4%, P = 0.0005), and a higher rate of annual eGFR decline (-4.3 ± 5.1 vs. 0.2 ± 4.6 mL/min/year, P = 0.01) than those without ACA. Univariate regression analysis and multivariate regression analysis adjusted for potential cofounders including age, eGFR, sex, diabetes mellitus, and hypertension showed that ACA was associated with eGFR decline (P = 0.011 and 0.017, respectively). Multivariate logistic regression analysis adjusted for these cofounders showed that ACA was associated with eGFR decline less than -4 mL/min/year (odds ratio 7.21, 95% confidence interval 0.93-56.1, P = 0.059).
  
  
  CONCLUSIONS
  ACA is an independent risk factor for CKD in PBC. Evaluation of ACA and kidney function is necessary to prevent CKD progression in PBC patients.
authors.affiliation: Department of Nephrology, Yokosuka Kyosai Hospital, 1-16 Yonegahamadori, Yokosuka, Kanagawa, 238-8558, Japan. shintaro_mandai@yahoo.co.jp
authors.forename: Shintaro
authors.initials: S
authors.lastname: Mandai
authors.forename: Eiichiro
authors.initials: E
authors.lastname: Kanda
authors.forename: Yohei
authors.initials: Y
authors.lastname: Arai
authors.forename: Suguru
authors.initials: S
authors.lastname: Hirasawa
authors.forename: Toshiyuki
authors.initials: T
authors.lastname: Hirai
authors.forename: Shota
authors.initials: S
authors.lastname: Aki
authors.forename: Naoto
authors.initials: N
authors.lastname: Inaba
authors.forename: Makoto
authors.initials: M
authors.lastname: Aoyagi
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Tanaka
authors.forename: Takaaki
authors.initials: T
authors.lastname: Ikeda
authors.forename: Teiichi
authors.initials: T
authors.lastname: Tamura
authors.forename: Sei
authors.initials: S
authors.lastname: Sasaki
mesh_terms: D000368:Aged; D000974:Antibodies, Antinuclear / Q000032:analysis*; D001323:Autoantibodies / Q000032:analysis*; D002503:Centromere / Q000276:immunology*; D018450:Disease Progression; D005260:Female; D005919:Glomerular Filtration Rate; D006801:Humans; D008105:Liver Cirrhosis, Biliary / Q000150:complications* / Q000276:immunology*; D008297:Male; D008875:Middle Aged; D051436:Renal Insufficiency, Chronic / Q000209:etiology*; D012189:Retrospective Studies; D012307:Risk Factors
chemical_list: D000974:Antibodies, Antinuclear; D001323:Autoantibodies