title: Cerebral ischemia as a causative mechanism for rapid progression of brain atrophy in chronic hemodialysis patients.
abstract: BACKGROUND
  It has been found that brain atrophy develops more rapidly in patients with end-stage renal failure after initiation of dialysis therapy. The present study was designed to analyze the relationship between brain atrophy and asymptomatic ischemic brain lesions.
  
  
  METHODS
  Magnetic resonance imaging (MRI) was performed for the evaluation of brain atrophy and ischemic lesions. Brain atrophy was assessed by the ventricular-brain ratio (VBR), calculated as the ratio of the ventricular area to the whole brain area on the maximum MRI slice. The severity of periventricular hyperintensity (PVH) and the number of lacunae were also regarded as ischemic brain lesions. Fifty-five patients undergoing maintenance hemodialysis (HD) without clinically overt neurological signs and symptoms, with a mean age of 52 +/- 11 (SD) years and a mean HD duration of 7 +/- 6 (SD) years were subjected. VBR and its relationship to ischemic brain lesion data were compared to those in 35 non-HD patients (controls), with a mean age of 42 +/- 14 (SD) years.
  
  
  RESULTS
  The VBR, the number of lacunae and the severity of PVH tended to increase with age in HD. The VBRs at all age groups were significantly higher in HD than in controls (7.0 vs 3.7% at the 4th decade, p < 0.05; 8.4 vs 5. 9% at the 5th decade, p < 0.05; 9.6 vs 5.4% at the 6th decade, p < 0.05; and 11.6 vs 6.3% at the 7th decade, p < 0.05). HD patients had significantly higher number of lacunae and had more advanced PVH than did controls. Both the number of lacunae and the severity of PVH were significantly correlated to VBR in HD.
  
  
  CONCLUSIONS
  In conclusion, the rapid progression of brain atrophy was related to the asymptomatic ischemic brain lesions in our HD patients. Such data indicated that cerebral ischemia might be a causative mechanism of brain atrophy in chronic hemodialysis patients.
authors.affiliation: Second Department of Internal Medicine, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Yoshimitsu
authors.forename: H
authors.initials: H
authors.lastname: Hirakata
authors.forename: K
authors.initials: K
authors.lastname: Fujii
authors.forename: H
authors.initials: H
authors.lastname: Kanai
authors.forename: E
authors.initials: E
authors.lastname: Hirakata
authors.forename: H
authors.initials: H
authors.lastname: Higashi
authors.forename: M
authors.initials: M
authors.lastname: Kubo
authors.forename: H
authors.initials: H
authors.lastname: Tanaka
authors.forename: M
authors.initials: M
authors.lastname: Shinozaki
authors.forename: R
authors.initials: R
authors.lastname: Katafuchi
authors.forename: Y
authors.initials: Y
authors.lastname: Yokomizo
authors.forename: Y
authors.initials: Y
authors.lastname: Oh
authors.forename: S
authors.initials: S
authors.lastname: Tomooka
authors.forename: S
authors.initials: S
authors.lastname: Fujimi
authors.forename: M
authors.initials: M
authors.lastname: Fujishima
mesh_terms: D001284:Atrophy; D001921:Brain / Q000473:pathology*; D002545:Brain Ischemia / Q000150:complications* / Q000473:pathology; D016022:Case-Control Studies; D005260:Female; D006801:Humans; D007674:Kidney Diseases / Q000628:therapy; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D006435:Renal Dialysis; D013997:Time Factors