Reduction in Estimated Glomerular Filtration Rate (eGFR) Results in an Increased Risk of Spontaneous Hemorrhagic Transformation in Patients with Large-artery Atherosclerosis Stroke
Reduction in Estimated Glomerular Filtration Rate (eGFR) Results in an Increased Risk of Spontaneous Hemorrhagic Transformation in Patients with Large-artery Atherosclerosis Stroke
复制标题
估计肾小球滤过率 (eGFR) 降低会导致大动脉粥样硬化性中风患者自发性出血性转化的风险增加
DOI：
10.2174/1567202612666151027151445
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发表时间：
2016-01-01
影响因子：
2.1
通讯作者：
Liu, Ming
中科院分区：
文献类型：
--
作者：
Liu, Bian;Wang, Deren;Liu, Ming
慢性肾脏病与急性缺血性卒中患者自发性出血性转化（HT）之间的关系很少有报道。我们进行这项研究的目的是确定估计肾小球滤过率 (eGFR) 降低是否与急性缺血性卒中患者的自发性 HT 相关，并检查这种关联是否取决于卒中病因。入院时血清肌酐水平可用的诊断为急性缺血性脑卒中的患者连续前瞻性地纳入成都脑卒中登记数据库。所有入院时均通过颅脑计算机断层扫描 (CT) 扫描进行分析，2-3 天后进行定期磁共振成像 (MRI) 分析，如果神经系统症状恶化，则进行 CT 扫描。 HT 是根据 MRI 或后来的 CT 定义的，eGFR 是使用肾病饮食修改方程计算的。进行单变量分析和多变量逻辑回归以确定 eGFR 降低（定义为 < 60 ml/min/1.73m2）是否与自发性 HT 相关。还在根据 Org 10172 急性中风治疗 (TOAST) 试验标准分类的患者亚组中评估了这种关联。在纳入的 1,645 名患者中，123 名 (7.5%) 出现自发性 HT，215 名 (13.1%) 出现 eGFR 降低。在所有缺血性卒中患者中，eGFR 降低与自发性 HT 风险增加显着相关（OR 1.821，95% CI 1.081 至 3.06，P=0.024），并且在大动脉粥样硬化亚组中，而非心源性栓塞卒中组中（OR 1.588，95% CI 0.642 至 3.782，P=0.024）。 P=0.327）。 eGFR 降低并不会增加症状性出血性转化的风险（OR 0.937，95%CI 0.247 至 3.577，P=0.924）。总之，在所有缺血性中风患者以及大动脉粥样硬化患者中，eGFR 降低与自发性 HT 风险增加显着相关，而在心源性栓塞中风患者中，eGFR 降低则与此无关。 eGFR 降低不会增加症状性 HT 的风险。
The association between chronic kidney disease and spontaneous hemorrhagic transformation (HT) in patients with acute ischemic stroke is seldom reported. We performed this study to identify whether reduced estimated glomerular filtration rate (eGFR) is associated with spontaneous HT in acute ischemic stroke patients, and examine whether the association depends on stroke etiology. Patients diagnosed with acute ischemic stroke whose serum creatinine levels at admission were available were consecutively and prospectively enrolled in the Chengdu Stroke Registry Database. All were analyzed on admission by cranial computed tomography (CT) scanning, followed by regular magnetic resonance imaging (MRI) 2-3 days later and afterwards CT scan if neurological symptoms deteriorated. HT was defined based on the MRI or later CT, and eGFR was calculated using the Modification of Diet in Renal Disease equation. Univariate analysis and multivariable logistic regression were performed to determine whether reduced eGFR, defined as < 60 ml/min/1.73m2, was associated with spontaneous HT. The association was also assessed in subgroups of patients classified according to the criteria of the Trial of Org 10172 in Acute Stroke Treatment (TOAST). Of the 1,645 patients enrolled, 123 (7.5%) developed spontaneous HT and 215 (13.1%) had reduced eGFR. Reduced eGFR was significantly associated with increased risk of spontaneous HT in all ischemic stroke patients (OR 1.821, 95% CI 1.081 to 3.06, P=0.024), and in the subgroup of large artery atherosclerosis, not in the cardio-embolism stroke group (OR 1.588, 95% CI 0.642 to 3.782, P=0.327). Reduced eGFR did not increase the risk of symptomatic hemorrhagic transformation (OR 0.937, 95%CI 0.247 to 3.577, P=0.924). In conclusion, reduced eGFR was significantly associated with increased risk of spontaneous HT in all ischemic stroke patients, and in large artery atherosclerosis, not in cardio-embolism stroke. Reduced eGFR did not increase the risk of symptomatic HT.