Cerebral blood flow and vasodilatory capacity in anemia secondary to chronic renal failure

Kuwabara, Yasuo; Sasaki, Masayuki; Hirakata, Hideki; Koga, Hirofumi; Nakagawa, Makoto; Chen, Tao; Kaneko, Koichiro; Masuda, Kouji; Fujishima, Masatoshi

doi:10.1046/j.1523-1755.2002.00142.x

Cited by 89 publications

(94 citation statements)

References 18 publications

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“…Similarly, Vorstrup et al (1992) reported that CBF in their hemodialysis patients was high owing to anemia, but when corrected to control Hct values was significantly reduced, suggesting metabolic reductions. Reduced CMRO 2 and slightly elevated OEF, with anemiaassociated hyperemia, in interdialytic day were also found by Kuwabara et al (2002). These previous results are consistent with our finding of CBF reductions by 19% (in interdialytic ASL-MRI studies) and 40% (ICA BF at the start of dialysis) in non-anemic hemodialysis patients.…”

Section: Discussionsupporting

confidence: 92%

Cerebrovascular Effects of Hemodialysis in Chronic Kidney Disease

Prohovnik

Post

Uribarri

et al. 2007

J Cereb Blood Flow Metab

161

165

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Patients with end-stage renal disease (ESRD) undergoing hemodialysis are known to suffer cognitive deficits and stroke of unknown etiology. It has been suspected that the treatment itself may contribute to the syndrome by unknown mechanisms, which we investigated in this study. Endstage renal disease patients on hemodialysis (n = 19) or peritoneal dialysis (PD, n = 5) were compared with 14 healthy controls. Subjects participated in magnetic resonance imaging (MRI) measurements of cerebral atrophy, cerebral blood flow (CBF) arterial spin labeled-MRI (ASL-MRI), quantitative Doppler blood flow through the internal carotid artery, and cerebral oxymetry. The Doppler and oxymetry procedures were also performed at the beginning and end of a single hemodialysis session. End-stage renal disease patients on hemodialysis showed significant cerebral atrophy, associated with longer hemodialysis duration and cognitive deficits, including focal bilateral lesions in the caudate nucleus and midbrain. Cerebral oxygenation was extremely low before dialysis (rSO 2 41613, compared with 7062 in controls, P < 0.02) and improved only slightly after dialysis. Carotid blood flow was also very low at the start of dialysis (115628 mL/sec, versus 193656 in controls, P < 0.005) but normalized at the end of the session (181 mL/sec). The PD patients showed intermediate values, between the hemodialysis and controls. Notably, duration of hemodialysis treatment predicted global gray-matter volume (r = À0.74), change of blood flow during dialysis (r = À0.65), and baseline rSO 2 (r = À0.65). The findings suggest that ESRD patients on hemodialysis suffer low CBF during the interdialytic cycle. Coupled with low cerebral oxygenation levels and atherosclerosis, this may contribute significantly to the etiology of the observed cerebral atrophy, cognitive deficits, and high stroke prevalence.

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Section: Discussionsupporting

confidence: 92%

Cerebrovascular Effects of Hemodialysis in Chronic Kidney Disease

Prohovnik

Post

Uribarri

et al. 2007

J Cereb Blood Flow Metab

161

165

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“…9 Different hemodynamic disturbances have been reported in patients with CKD. 10,11 Nevertheless, it is not clear whether impaired kidney function is associated with lower cerebral blood flow in the general population. Therefore, we aimed to investigate the association between different measures of kidney function and cerebral blood flow in a population-based cohort of individuals 45 years old and older.…”

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confidence: 99%

Kidney Function and Cerebral Blood Flow

Sedaghat¹,

Vernooij

Loehrer³

et al. 2016

Journal of the American Society of Nephrology

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CKD is linked with various brain disorders. Whereas brain integrity is dependent on cerebral perfusion, the association between kidney function and cerebral blood flow has yet to be determined. This study was performed in the framework of the population-based Rotterdam Study and included 2645 participants with mean age of 56.6 years (45% men). We used eGFR and albumin-to-creatinine ratio to assess kidney function and performed phase-contrast magnetic resonance imaging of basilar and carotid arteries to measure cerebral blood flow. Participants had an average (SD) eGFR of 86.3 (13.4) ml/min per 1.73 m 2 and a median (interquartile range) albumin-to-creatinine ratio of 3.4 (2.2-6.1) mg/g.In age-and sex-adjusted models, a higher albumin-to-creatinine ratio was associated with lower cerebral blood flow level (difference in cerebral blood flow [milliliters per minute per 100 ml] per doubling of the albumin-to-creatinine ratio, 20.31; 95% confidence interval, 20.58 to 20.03). The association was not present after adjustment for cardiovascular risk factors (P=0.10). Each 1 SD lower eGFR was associated with 0.42 ml/min per 100 ml lower cerebral blood flow (95% confidence interval, 0.01 to 0.83) adjusted for cardiovascular risk factors. Thus, in this population-based study, we observed that lower eGFR is independently associated with lower cerebral blood flow.

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“…5 Interestingly, an animal study suggested that myogenic constriction of cerebral arteries is impaired in uremic hypertensive rats. 8 In addition, a human study demonstrated that cerebral vasodilatory capacity is decreased in patients with anemia secondary to chronic renal failure, 9 indicating that anemia deserves more attention, although hematologic findings have rarely been described in this syndrome. 3 Considering the frequent occurrence of peridialytic blood pressure changes, 10 it is tempting to speculate that blood pressure changes contribute to failed autoregulation of perforating arteries, resulting in edematous lentiform nucleus lesions in cases of long-term kidney failure, particularly in those with diabetes and anemia.…”

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confidence: 99%

Mystery Case: Parkinsonism in a diabetic uremic patient

et al. 2016

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A 71-year-old man noticed a sudden feeling of weakness in the limbs after a routine hemodialysis session, and was admitted to the hospital. He had a history of hypertension and diabetes mellitus for approximately 20 years and diabetic nephropathy requiring hemodialysis for over 1 year. He was taking metformin, which was changed from sulfonylurea 2 months before. His consciousness level deteriorated 1 day after symptom onset, and laboratory examination revealed a blood glucose level of 42 mg/dL. His level of consciousness improved after glycemic treatment, but the weakness did not. MRI of the brain revealed abnormalities in the bilateral basal ganglia (figure e-1 on the Neurology ® Web site at Neurology.org).The patient was referred to our hospital 8 days after symptom onset. Neurologic examination revealed normal consciousness, symmetric rigid-akinetic parkinsonism (rigidity of the neck and limbs, akinesia, severe postural instability, Myerson sign, and absence of tremor), proximal muscle weakness, bilateral hyperreflexia, and bilateral Babinski signs. Blood tests were as follows: hemoglobin 9.8 g/dL, hematocrit 32.9%, mean corpuscular volume 83.1 fL, blood urea nitrogen 44 mg/dL, creatinine 9.2 mg/dL, sodium 134 mEq/L, potassium 4.0 mEq/L, calcium 8.8 mg/dL, inorganic phosphorus 4.7 mg/dL (reference range 2.5-4.5 mg/dL), magnesium 3.0 mg/dL (reference range 1.9-2.5 mg/dL), iron 26 mg/dL (reference range 60-210 mg/dL), glucose 158 mg/dL, and HbA1c 6.1%. Brain MRI (3.0T) acquired 10 days after symptom onset demonstrated edematous changes in the basal ganglia bilaterally, particularly in the putamen and globus pallidus ( figure 1A). Abnormalities in the bilateral globus pallidus on diffusion-weighted imaging and apparent diffusion coefficient (ADC) map were less evident than they were on the initial MRI ( figure 1, B and C). Of note, pseudocontinuous arterial spin labeling (pCASL), which is a perfusion imaging technique without contrast media use, revealed marked hyperperfusion in the bilateral basal ganglia ( figure 1D), accompanied by dilated perforating branches, or lenticulostriate arteries (figure 1, E and F).

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Cerebral blood flow and vasodilatory capacity in anemia secondary to chronic renal failure

Abstract: The present study revealed the existence of a reduced cerebral vasodilatory capacity in anemic patients with CRF, suggesting that chronic hypoxic brain damage might play a role in the impaired cerebrovascular response to CO2.

Cited by 89 publications

References 18 publications

Cerebrovascular Effects of Hemodialysis in Chronic Kidney Disease

Cerebrovascular Effects of Hemodialysis in Chronic Kidney Disease

Kidney Function and Cerebral Blood Flow

Mystery Case: Parkinsonism in a diabetic uremic patient

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