Introduction Chronic Kidney Disease (CKD) patients experience an elevated risk for cerebrovascular disease and neurocognitive dysfunction. One mechanism that may contribute to this heightened risk is an impairment in dynamic cerebral autoregulation; the ability of cerebral vessels to stabilize changes in cerebral blood flow during fluctuations in arterial pressure. We compared dynamic cerebral autoregulation between patients with CKD stages III‐IV, and controls (CON) without CKD matched for age, race, sex, and anti‐hypertensive medication use. We hypothesized that dynamic cerebral autoregulation would be impaired in CKD compared to CON. Methods 12 CKD participants (age=63±3y, eGFR=40±3 mL/min/1.73m 2 ), and 16 CON participants (age=58±2y), performed 2, 5‐minute bouts of repeated sit‐to‐stand maneuvers at 0.05Hz (10‐s sit, 10‐s stand) and 0.10Hz (5‐s sit, 5‐s stand) which correspond to the frequency ranges in which cerebral autoregulation is operant. The order of protocols was randomized and separated by a 5‐minute rest period. Heart rate (via ECG), arterial pressure (via finger photoplethysmography), middle cerebral artery velocity (MCAv; via transcranial Doppler ultrasonography), and end‐tidal carbon dioxide (etCO 2 ) were measured continuously throughout both protocols. Dynamic cerebral autoregulation was characterized by performing a transfer function analysis on the mean arterial pressure‐middle cerebral artery velocity (MAP‐MCAv) relationship to derive coherence, phase, and gain. MAP‐MCAv coherence, phase, and gain were compared between groups during each of the 2 maneuvers via unpaired, 2‐tailed T‐tests. Results As expected, MAP‐MCAv coherence approached 1.0 during both maneuvers (≥0.8 during 0.05Hz and ≥0.6 during 0.10Hz) with no differences between groups (P≥0.60) supporting reliability of phase and gain measures. We observed no group differences in MAP‐MCAv phase or gain during the 0.05Hz maneuver (Phase: CKD=1.4±0.09, CON=1.2±0.07, P=0.14; Gain: CKD=0.70±0.07, CON=0.75±0.05, P=0.59) suggesting no impairment in the myogenic component of cerebral autoregulation in CKD. Not all participants were able to perform the 0.10Hz maneuver due to musculoskeletal limitations, thus N=6 CKD and N=12 CON during 0.10Hz repeated sit‐to‐stand. Similarly, we observed no group differences in phase or gain measurements during the 0.10Hz maneuver (Phase: CKD=1.4±0.12, CON=1.3±0.09, P=0.35; Gain: CKD=0.69±0.08, CON=0.88±0.06, P=0.11) suggesting no impairment in the neurogenic component of cerebral autoregulation in CKD. Discussion Contrary to our hypothesis, we observed no impairment in cerebral autoregulation in CKD stages III‐IV. These findings suggest that other mechanisms likely contribute to the increased cerebrovascular disease risk observed in CKD. Future work should explore the role of other cerebrovascular regulatory mechanisms such as cerebrovascular CO 2 reactivity and neurovascular coupling as potential mediators of the increased cerebrovascular disease risk exhibited in CKD.