流行病学数据表明,在慢性肾脏病的所有阶段个体都有更高的风险发展成神经精神疾病、认知障碍和痴呆。这一危险的现象通常可以用症状性和亚临床性缺血性脑血管病变的高发来解释。潜在的机制包括细胞因子/趋化因子的释放、活性氧的产生、营养因子的循环和局部形成以及与肾素-血管紧张素系统相关的分子。作者综述了实验和临床证据的作用,以及这些机制在肾脑之间的交互作用。了解肾脏损害和大脑功能之间的病理生理相互作用,对于降低未来认知损害的风险和开发新的药物治疗策略具有重要意义。

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