Cerebral ischemia as a causative mechanism for rapid progression of brain atrophy in chronic hemodialysis patients

Citation
T. Yoshimitsu et al., Cerebral ischemia as a causative mechanism for rapid progression of brain atrophy in chronic hemodialysis patients, CLIN NEPHR, 53(6), 2000, pp. 445-451
Citations number
22
Categorie Soggetti
Urology & Nephrology","da verificare
Journal title
CLINICAL NEPHROLOGY
ISSN journal
03010430 → ACNP
Volume
53
Issue
6
Year of publication
2000
Pages
445 - 451
Database
ISI
SICI code
0301-0430(200006)53:6<445:CIAACM>2.0.ZU;2-D
Abstract
Background: It has been found that brain atrophy develops more rapidly in p atients with end-stage renal failure after initiation of dialysis therapy. The present study was designed to analyze the relationship between brain at rophy and asymptomatic ischemic brain lesions. Patients and methods: Magnet ic resonance imaging (MRI) was performed for the evaluation of brain atroph y 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 hyperi ntensity (PVH) and the number of lacunae were also regarded as ischemic bra in lesions. Fifty-five patients undergoing maintenance hemodialysis (HD) wi thout 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 subj ected. 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 (S D) years. Results: The VBR, the number of lacunae and the severity of PVH t ended to increase with age in HD. The VBRs at all age groups were significa ntly 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 si gnificantly higher number of lacunae and had more advanced PVH than did con trols. Both the number of lacunae and the severity of PVH were significantl y correlated to VBR in HD. Conclusion: 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 cau sative mechanism of blain atrophy in chronic hemodialysis patients.