Depressed cerebral oxygen metabolism in patients with chronic renal failure: A positron emission tomography study

Citation
H. Kanai et al., Depressed cerebral oxygen metabolism in patients with chronic renal failure: A positron emission tomography study, AM J KIDNEY, 38(4), 2001, pp. S129-S133
Citations number
20
Categorie Soggetti
Urology & Nephrology
Journal title
AMERICAN JOURNAL OF KIDNEY DISEASES
ISSN journal
02726386 → ACNP
Volume
38
Issue
4
Year of publication
2001
Supplement
1
Pages
S129 - S133
Database
ISI
SICI code
0272-6386(200110)38:4<S129:DCOMIP>2.0.ZU;2-N
Abstract
To elucidate brain oxygen metabolism in uremic patients, regional cerebral blood flow (rCBF), oxygen extraction (rOEF), and oxygen metabolism (rCMRO(2 )) were measured by positron emission tomography (PET) in 10 hemodialysis ( HD) patients and 13 predialysis patients with chronic renal failure (CRF). Data were compared with 20 nonuremic patients (controls) without neurologic al abnormalities, congestive heart failure, history of cerebrovascular acci dent, diabetes mellitus, or symptomatic brain lesion on magnetic resonance imaging. In the hemisphere, rCMRO(2) in both HD (1.82 +/- 0.10 mL/min/100 g ) and CRF patients (1.95 +/- 0.09 mL/min/100 g) showed significantly lower values compared with controls (2.23 +/- 0.05 mL/min/100 9; P < 0.01). Hemis pheric rCBF in HD (35.6 +/- 2.1 mL/100 g/min) and CRF patients (36.1 +/- 2. 1 mL/100 g/min)was not different from controls(31.8 +/- 1.4 mL/100 g/min). Hemispheric rOEF in CRF patients (45.7% +/- 1.6%) was significantly greater than that in controls (40.5% +/- 1.2%; P < 0.02), but rOEF in HD patients (43.7% +/- 1.9%) did not increase significantly. These tendencies were simi lar in all regions of interest, especially cerebral cortices. All PET param eters in frontal cortices tended to show the lowest values In patients with renal failure. For all HD patients, rCBF in both the frontal cortex and wh ite matter correlated inversely with HD therapy duration (P < 0.05). In con clusion, brain oxygen metabolism is depressed in patients with renal failur e on or before the start of HD therapy. The cause for depressed brain oxyge n metabolism is considered to be either dysregulation of cerebral circulati on or lower brain cell activity. (C) 2001 by the National Kidney Foundation , Inc.