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Kidney Week

Abstract: PO1829

Cerebrovascular Dysfunction in CKD

Session Information

Category: Hypertension and CVD

  • 1403 Hypertension and CVD: Mechanisms

Authors

  • Steele, Cortney, University of Colorado - Anschutz Medical Campus, Aurora, Colorado, United States
  • Oh, Ester, University of Colorado - Anschutz Medical Campus, Aurora, Colorado, United States
  • Farmer-Bailey, Heather, University of Colorado - Anschutz Medical Campus, Aurora, Colorado, United States
  • Reddin, Rachael L., University of Colorado - Anschutz Medical Campus, Aurora, Colorado, United States
  • Struemph, Taylor, University of Colorado - Anschutz Medical Campus, Aurora, Colorado, United States
  • Chonchol, Michel, University of Colorado - Anschutz Medical Campus, Aurora, Colorado, United States
  • Nowak, Kristen L., University of Colorado - Anschutz Medical Campus, Aurora, Colorado, United States
Background

Cerebrovascular dysfunction, characterized by reduced cerebrovascular reactivity, cerebral hypoperfusion, and increased pulsatile flow within the brain precedes the onset of dementia and is linked to cognitive dysfunction. While large-artery vascular dysfunction is prevalent in chronic kidney disease (CKD), cerebrovascular function has not been well characterized to date in moderate-to-severe CKD.

Methods

Using transcranial Doppler, we compared middle cerebral artery (MCA) blood flow-velocity response to hypercapnia (normalized for blood pressure and end-tidal CO2; a measure of cerebrovascular reactivity) and MCA pulsatility (a measure of cerebrovascular stiffness) in patients with stage 3-4 CKD vs. age-matched healthy controls using an independent samples t-test. We also administered the trail making test (parts A and B) as an index of processing speed and measured carotid-femoral pulse-wave velocity (CFPWV) as an index of aortic stiffness.

Results

Seven participants with CKD (2F, 68±3 yrs [mean±s.e.m.], estimated glomerular filtration rate [eGFR]: 38±5 ml/min/1.73m2) were compared to 8 healthy controls (1F, 63±2 yrs, eGFR: 83±5 ml/min/1.73m2). MCA pulsatility index was greater (1.08±0.10 vs. 0.85±0.04 A.U.; p<0.05) and normalized MCA blood flow-velocity response to hypercapnia tended to be lower (-6.3±4.0 vs. 11.6±7.3 %; p=0.06) in CKD as compared to healthy controls. Trail making part A time was slower (A: 31.8±3.3 vs. 20.2±1.6 sec; p<0.01); part B time tended to be slower (longer time to complete): 71.7±13.6 vs. 42.7±6.7 sec; p=0.07) and CFPWV was greater (1122±115 vs. 811±88 cm/sec; p<0.05) in CKD vs. control. Greater MCA pulsatility index correlated with worse cerebrovascular reactivity (r = -0.63, p=0.01), greater CFPWV (r= 0.65, p<0.01), slower trail making part B time (r =0.59, p<0.05), and lower eGFR (r = -0.53, p=0.09).

Conclusion

Impaired cerebrovascular function is evident in patients with moderate-to-severe CKD. Increased cerebrovascular stiffness is associated with reduced kidney function, increased aortic stiffness, impaired processing speed, and worse cerebrovascular reactivity.