Miranda Aline Silva, Cordeiro Thiago Macedo, Dos Santos Lacerda Soares Thomas Mucida, Ferreira Rodrigo Novaes, Simões E Silva Ana Cristina
Laboratório de Neurobiologia, Departamento de Morfologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais (UFMG), Brazil.
Laboratório Interdisciplinar de Investigação Médica (LIIM), Faculdade de Medicina, UFMG, Belo Horizonte, Brazil.
Clin Sci (Lond). 2017 Jun 1;131(11):1093-1105. doi: 10.1042/CS20160927.
Epidemiologic data suggest that individuals at all stages of chronic kidney disease (CKD) have a higher risk of developing neuropsychiatric disorders, cognitive impairment, and dementia. This risk is generally explained by the high prevalence of both symptomatic and subclinical ischemic cerebrovascular lesions. However, other potential mechanisms, including cytokine/chemokine release, production of reactive oxygen species (ROS), circulating and local formation of trophic factors and of renin-angiotensin system (RAS) molecules, could also be involved, especially in the absence of obvious cerebrovascular disease. In this review, we discuss experimental and clinical evidence for the role of these mechanisms in kidney-brain cross-talk. In addition, we hypothesize potential pathways for the interactions between kidney and brain and their pathophysiological role in neuropsychiatric and cognitive changes found in patients with CKD. Understanding the pathophysiologic interactions between renal impairment and brain function is important in order to minimize the risk for future cognitive impairment and to develop new strategies for innovative pharmacological treatment.
流行病学数据表明，慢性肾脏病（CKD）各个阶段的个体发生神经精神障碍、认知障碍和痴呆的风险更高。这种风险通常由有症状和亚临床缺血性脑血管病变的高患病率来解释。然而，其他潜在机制，包括细胞因子/趋化因子释放、活性氧（ROS）生成、营养因子以及肾素-血管紧张素系统（RAS）分子的循环和局部形成，也可能参与其中，尤其是在没有明显脑血管疾病的情况下。在本综述中，我们讨论了这些机制在肾-脑相互作用中作用的实验和临床证据。此外，我们推测了肾脏与大脑之间相互作用的潜在途径及其在CKD患者神经精神和认知变化中的病理生理作用。了解肾功能损害与脑功能之间的病理生理相互作用对于将未来认知障碍的风险降至最低以及开发创新药物治疗的新策略非常重要。
