Chronic kidney disease (CKD) and end-stage kidney disease (ESKD) patients experience an increased risk of cerebrovascular disease and cognitive dysfunction. Hemodialysis (HD), a major modality of renal replacement therapy in ESKD, can cause rapid changes in blood pressure, osmolality, and acid-base balance that collectively present a unique stress to the cerebral vasculature. This review presents an update regarding cerebral blood flow (CBF) regulation in CKD and ESKD, and how the maintenance of cerebral oxygenation may be compromised during HD. ESKD patients exhibit decreased cerebral oxygen delivery due to anemia, despite cerebral hyperperfusion at rest. Cerebral oxygenation further declines during HD due to reductions in CBF, and this may induce cerebral ischemia or "stunning". Intradialytic reductions in CBF are driven by decreases in cerebral perfusion pressure that may be partially opposed by bicarbonate shifts during dialysis. Intradialytic reductions in CBF have been related to several variables that are routinely measured in clinical practice including ultrafiltration rate and blood pressure. However, the role of compensatory cerebrovascular regulatory mechanisms during HD remain relatively unexplored. In particular, cerebral autoregulation can oppose reductions in CBF driven by reductions in systemic blood pressure, while cerebrovascular reactivity to CO₂ may attenuate intradialytic reductions in CBF through promoting cerebral vasodilation. However, whether these mechanisms are effective in ESKD and during HD remain relatively unexplored. Important areas for future work include investigating potential alterations in cerebrovascular regulation in CKD and ESKD, and how key regulatory mechanisms are engaged and integrated during HD to modulate intradialytic declines in CBF.

中文翻译：

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终末期肾脏疾病中的脑血流调节

慢性肾脏病（CKD）和终末期肾脏病（ESKD）患者的脑血管疾病和认知功能障碍的风险增加。血液透析（HD）是ESKD中肾脏替代治疗的主要方式，可引起血压，重量克分子渗透压浓度和酸碱平衡的快速变化，共同对脑血管系统造成独特的压力。这篇综述介绍了有关CKD和ESKD中脑血流（CBF）调节的最新信息，以及在HD期间如何损害脑氧合的维持。尽管休息时大脑过度灌注，但由于贫血，ESKD患者仍表现出减少的脑氧输送。HD期间由于CBF的减少，脑氧合进一步下降，这可能会诱发脑缺血或“令人震惊”。透析中脑内血流压力的降低可能导致透析液中CBF的降低，而脑血流灌注压力的降低可能与透析过程中碳酸氢盐的移动部分抵消。透析中CBF的降低与临床实践中常规测量的几个变量有关，包括超滤率和血压。然而，在HD期间代偿性脑血管调节机制的作用仍未被探索。尤其是，脑自动调节可以反对由于全身血压降低而导致的CBF降低，而脑血管对CO的反应性 透析中CBF的降低与临床实践中常规测量的几个变量有关，包括超滤率和血压。然而，在HD期间代偿性脑血管调节机制的作用仍未被探索。尤其是，脑自动调节可以反对由于全身血压降低而导致的CBF降低，而脑血管对CO的反应性 透析中CBF的降低与临床实践中常规测量的几个变量有关，包括超滤率和血压。然而，在HD期间代偿性脑血管调节机制的作用仍未被探索。尤其是，脑自动调节可以反对由于全身血压降低而导致的CBF降低，而脑血管对CO的反应性₂可能通过促进脑血管舒张而减弱CBF的透析内减少。但是，这些机制在ESKD中和HD期间是否有效尚待进一步研究。未来工作的重要领域包括调查CKD和ESKD中脑血管调节的潜在变化，以及在HD期间如何参与和整合关键调节机制以调节CBF的透析内下降。