From the Wolfson Center for Prevention of Stroke and Dementia, Nuffield Department of Clinical Neurosciences, John Radcliffe Hospital, University of Oxford, UK.
Neurology. 2022 Feb 15;98(7):e711-e720. doi: 10.1212/WNL.0000000000013205. Epub 2022 Jan 7.
Individuals with chronic kidney disease (CKD) appear to be at increased risk of cognitive impairment, with both vascular and neurodegenerative mechanisms postulated. To explore the vascular hypothesis, we studied the association between CKD and dementia before and after TIA and stroke.
In a prospective, population-based cohort study of TIA and stroke (Oxford Vascular Study; 2002-2012), pre-event and new postevent dementia were ascertained through direct patient assessment and follow-up for 5 years, supplemented by review of hospital/primary care records. Associations between pre-event dementia and CKD (defined as an estimated glomerular filtration rate [eGFR] <60 mL/min/1.73 m) were examined using logistic regression and between postevent dementia and CKD using Cox and competing risk regression models, adjusted for age, sex, education, stroke severity, prior stroke, white matter disease, diabetes mellitus, and dysphasia.
Among 2,305 patients with TIA/stroke (median [interquartile range] age, 77 [67-84] years, 1,133 [49%] male, 688 [30%] TIA), 1,174 (50.9%) had CKD. CKD was associated with both pre-event (odds ratio [OR] 2.04 [95% confidence interval (CI) 1.52-2.72]; < 0.001) and postevent dementia (hazard ratio [HR] 2.01 [95% CI 1.65-2.44]; < 0.001), but these associations attenuated after adjustment for covariates (OR 0.92 [0.65-1.31]; = 0.65 and HR 1.09 [0.85-1.39]; = 0.50). The results were similar when a competing risk model was used (subdistribution HR [SHR] 1.74 [1.43-2.12]; < 0.001, attenuating to 1.01 [0.78-1.33]; = 0.92 with adjustment). CKD was more strongly associated with late (>1 year) postevent dementia (SHR 2.32 [1.70-3.17]; < 0.001), particularly after TIA and minor stroke (SHR 3.08 [2.05-4.64]; < 0.001), but not significantly so after adjustment (SHR 1.53 [0.90-2.60]; = 0.12).
In patients with TIA and stroke, CKD was not independently associated with either pre- or postevent dementia, suggesting that renal-specific mechanisms are unlikely to play an important role in aetiology.
患有慢性肾脏病（CKD）的个体似乎存在认知障碍的风险增加，推测存在血管和神经退行性机制。为了探索血管假说，我们研究了 TIA 和中风前后 CKD 与痴呆之间的关联。
在一项前瞻性、基于人群的 TIA 和中风研究（牛津血管研究；2002-2012 年）中，通过直接患者评估和 5 年的随访确定事件前和新发生的痴呆，通过查看医院/初级保健记录进行补充。使用逻辑回归检查事件前痴呆与 CKD（定义为估计肾小球滤过率[eGFR]＜60mL/min/1.73m）之间的关联，并使用 Cox 和竞争风险回归模型检查事件后痴呆与 CKD 之间的关联，调整了年龄、性别、教育程度、中风严重程度、既往中风、白质疾病、糖尿病和言语障碍。
在 2305 例 TIA/中风患者（中位数[四分位数范围]年龄为 77[67-84]岁，1133[49%]为男性，688[30%]为 TIA）中，有 1174 例（50.9%）患有 CKD。CKD 与事件前（优势比[OR]2.04[95%置信区间（CI）1.52-2.72]；＜0.001）和事件后痴呆（风险比[HR]2.01[95%CI 1.65-2.44]；＜0.001）均相关，但这些关联在调整协变量后减弱（OR 0.92[0.65-1.31]；=0.65 和 HR 1.09[0.85-1.39]；=0.50）。当使用竞争风险模型时，结果相似（亚分布 HR[SHR]1.74[1.43-2.12]；＜0.001，调整后为 1.01[0.78-1.33]；=0.92）。CKD 与晚期（＞1 年）事件后痴呆的相关性更强（SHR 2.32[1.70-3.17]；＜0.001），尤其是在 TIA 和小中风后（SHR 3.08[2.05-4.64]；＜0.001），但调整后并不显著（SHR 1.53[0.90-2.60]；=0.12）。
在 TIA 和中风患者中，CKD 与事件前或事件后痴呆均无独立关联，提示肾脏特异性机制不太可能在发病机制中发挥重要作用。
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