Cerebral blood flow decreases during intermittent hemodialysis in patients with acute kidney injury, but not in patients with end-stage renal disease.
BACKGROUND
Cerebral blood flow (CBF) may decrease during intermittent hemodialysis (IHD). Patients with acute kidney injury (AKI) may be more vulnerable to cerebral hypoperfusion than patients with end-stage renal disease (ESRD), due to concomitant critical illness and hemodynamic instability.


METHODS
In this observational, prospective study, we measured mean flow velocity at the level of the middle cerebral artery by transcranial Doppler at the start, after 2 h and at the end of a hemodialysis session in 15 consecutive patients with AKI and critical illness referred to the nephrological intensive care unit of a university hospital and in 12 patients with ESRD on regular treatment thrice weekly, who served as controls. We compared end-dialysis changes from baseline in mean flow velocity between the study groups and examined the correlation between this change and that of other relevant clinical parameters.


RESULTS
Mean flow velocity decreased significantly at end-dialysis in the patients with AKI, but not in those with ESRD (P = 0.02). This difference persisted after adjusting for baseline mean flow velocity and net ultrafiltration volume. No significant correlations were found in either group between changes in mean flow velocity and changes in mean blood pressure (AKI: r = -0.27, P = 0.34; ESRD: r = 0.15, P = 0.68), SUN (AKI: r = -0.33, P = 0.25; ESRD: r = 0.06, P = 0.85), plasma HCO(3)(-) (AKI: r = -0.52, P = 0.24; ESRD: r = -0.18, P = 0.59), hematocrit (AKI: r = 0.08, P = 0.71; ESRD: r = -0.19, P = 0.65) or arterial oxygen content (AKI: r = -0.17, P = 0.36; ESRD: r = -0.33, P = 0.43).


CONCLUSIONS
Our data suggest that AKI patients may be more vulnerable than ESRD patients to cerebral hypoperfusion during IHD. Our findings do not support a clear-cut role of rapid changes in blood osmolarity, rheological properties or vasoreactivity of the cerebral circulation to O(2) supply in modulating CBF during hemodialysis.
Department of Internal Medicine, Nephrology and Health Sciences, University of Parma Medical School, Via Gramsci 14, 43100 Parma, Italy. giuregolisti@gmail.com
Giuseppe
G
Regolisti
Umberto
U
Maggiore
Carola
C
Cademartiri
Aderville
A
Cabassi
Alberto
A
Caiazza
Stefano
S
Tedeschi
Elio
E
Antonucci
Enrico
E
Fiaccadori
D058186:Acute Kidney Injury / Q000503:physiopathology* / Q000628:therapy; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D062186:Arterial Pressure; D001783:Blood Flow Velocity; D002560:Cerebrovascular Circulation / Q000502:physiology*; D005260:Female; D006801:Humans; D007676:Kidney Failure, Chronic / Q000503:physiopathology* / Q000628:therapy; D008297:Male; D008875:Middle Aged; D020768:Middle Cerebral Artery / Q000000981:diagnostic imaging / Q000503:physiopathology*; D011446:Prospective Studies; D006435:Renal Dialysis; D017585:Ultrasonography, Doppler, Transcranial