Rob P M, Niederstadt C, Reusche E
Nephrologisches Zentrum am Klinikum Süd, Kalhlhorststrasse 31, D-23552 Lübeck, Germany.
CNS Drugs. 2001;15(9):691-9. doi: 10.2165/00023210-200115090-00003.
Dementia in patients undergoing long-term dialysis has not been clearly defined; however, four different entities have been described. Uraemic encephalopathy is a complication of uraemia and responds well to dialysis. Dialysis encephalopathy syndrome, the result of acute intoxication of aluminium caused by the use of an aluminium-containing dialysate, was a common occurrence prior to 1980. However, using modern techniques of water purification, such acute intoxication can now be avoided. Dialysis-associated encephalopathy/dementia (DAE) is always associated with elevated serum aluminium levels. Pathognomonic morphological changes in the brain have been described, but the mechanism for the entry of aluminium into the CNS is incompletely understood. The mechanisms involved in the pathogenesis of the neurotoxicity associated with aluminium are numerous. Although only a very small fraction of ingested aluminium is absorbed, the continuous oral aluminium intake from aluminium-based phosphate binders, and also of dietary or environmental origin, is responsible for aluminium overload in dialysis patients. Age-related dementia, especially vascular dementia, occurs in patients undergoing long-term dialysis as frequently as it does in the general population. The differential diagnoses of dialysis-associated dementias should include investigation for metabolic encephalopathies, heavy metal or trace element intoxications, and distinct structural neurological lesions such as subdural haematoma, normal pressure hydrocephalus, stroke and, particularly, hypertensive encephalopathy and multi-infarct dementia. To prevent DAE, dietary training programmes should aim to achieve the lowest phosphate intake and pharmacological tools should be used to keep serum phosphate levels below 2 mmol/L. To prevent vascular dementia, lifestyle modification should be undertaken, including optimal physical activity and fat intake, nicotine abstinence, and targeting optimal blood glucose, cholesterol and triglyceride levels, and blood pressure, to those outlined in current recommendations.
长期透析患者的痴呆症尚未有明确定义；然而，已描述了四种不同类型。尿毒症脑病是尿毒症的一种并发症，对透析反应良好。透析脑病综合征是使用含铝透析液导致铝急性中毒的结果，在1980年之前很常见。然而，采用现代水净化技术，现在可以避免这种急性中毒。透析相关性脑病/痴呆症（DAE）总是与血清铝水平升高相关。大脑中已描述了特征性的形态学变化，但铝进入中枢神经系统的机制尚不完全清楚。与铝相关的神经毒性发病机制涉及众多因素。尽管摄入的铝只有极小一部分被吸收，但来自铝基磷酸盐结合剂的持续口服铝摄入，以及饮食或环境来源的铝摄入，是透析患者铝过载的原因。与年龄相关的痴呆症，尤其是血管性痴呆症，在长期透析患者中的发生率与普通人群一样高。透析相关性痴呆症的鉴别诊断应包括对代谢性脑病、重金属或微量元素中毒以及明显的结构性神经病变（如硬膜下血肿、正常压力脑积水、中风，特别是高血压脑病和多发梗死性痴呆）的检查。为预防DAE，饮食训练计划应旨在实现最低的磷酸盐摄入量，并应使用药物工具将血清磷酸盐水平保持在2 mmol/L以下。为预防血管性痴呆症，应进行生活方式的改变，包括最佳的体育活动和脂肪摄入、戒烟，并将血糖、胆固醇和甘油三酯水平以及血压控制在当前建议所概述的最佳水平。
