Abstract
In order to elucidate brain oxygen metabolism in uremic patients, the regional cerebral blood flow (rCBF), oxygen extraction (rOEF) and oxygen metabolism (rCMRO2) were measured by positron emission tomography (PET) in both 10 hemodialysis patients (HD: male [m]/female [f]=2/8, age of 49±3 [SEM] years old, HD duration of 113±26 months) and 13 pre-dialysis renal failure patients (CRF: m/f=10/3, age of 61±2 years old, serum creatinine (SCr) of 6.3±1.0mg/dl). Data were compared with 20 non-uremic subjects (Control: m/f=7/13, age of 62±2 years old, SCr of 0.9±0.1mg/dl). They had no neurological abnormalities, congestive heart failure, history of cerebrovascular accident, diabetes mellitus, or symptomatic brain lesion on magnetic resonance imaging. The age of HD was significantly younger than the other groups (p<0.02) and the hemoglobin (Hb) levels in both HD (10.5±0.5g/dl) and CRF (9.8±0.9) were significantly lower than that in Control (13.3±0.3) (p<0.02).
In the hemisphere, rCMRO2 in both HD (1.82±0.10ml/min/100g) and CRF (1.95±0.09) showed significantly lower values as compared to Control (2.23±0.05) (p<0.01, respectively). Hemispheric rCBF in HD (35.6±2.1ml/100g/min) and in CRF (36.1±2.1) were not different from that in Control (31.8±1.4). Hemispheric rOEF in CRF (45.7±1.6%) was significantly higher than that in Control (40.5±1.2%) (p<0.02), but that in HD (43.7±1.9%) did not increase significantly. These tendencies were similar in all regions of interest, especially in the cerebral cortices, but not in the cerebellum. All PET parameters in the frontal cortices tended to show the lowest value in renal failure patients. For all HD patients, rCBF in both the frontal cortex and the white matter correlated inversely with HD duration (frontal cortex: r=-0.649, p<0.05; white matter: r=-0.706, p<0.02).
Based on these data, it is concluded that brain oxygen metabolism is depressed in renal failure patients on or before hemodialysis treatment. The cause for the depressed brain oxygen metabolism is considered to be due either to the dysregulation of cerebral circulation or to lower brain cell activity.
