Impact of Renal Impairment on Intensive Blood-Pressure-Lowering Therapy and Outcomes in Intracerebral Hemorrhage: Results From ATACH-2.
Impact of Renal Impairment on Intensive Blood-Pressure-Lowering Therapy and Outcomes in Intracerebral Hemorrhage: Results From ATACH-2.
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DOI：
10.1212/wnl.0000000000012442
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发表时间：
2021-08-31
期刊：
影响因子：
9.9
通讯作者：
Toyoda K
中科院分区：
文献类型：
--
作者：
Fukuda-Doi M;Yamamoto H;Koga M;Doi Y;Qureshi AI;Yoshimura S;Miwa K;Ishigami A;Shiozawa M;Omae K;Ihara M;Toyoda K
肾损害对脑出血(ICH)的临床影响尚不清楚。这项研究试图评估估计的肾小球滤过率(EGFR)是否会影响临床结果，或者是否会改变脑出血患者强化收缩压(BP)控制的有效性(目标为110-139 mm Hg)，而不是标准的(目标为140-179 mm Hg)。我们对ATACH-2进行了事后分析，这是一项随机的、两组的开放标签试验。使用慢性肾脏疾病流行病学协作方程计算每个符合条件的患者的基线EGFR。感兴趣的结果是90天时死亡或残疾。采用多因素Logistic回归模型进行分析。在随机抽取的1000名患者中，有974人进行了分析。≥-90、60-89和60mL/min/1.73m2分别为451例(46.3%)、363例(37.3%)和160例(16.4%)。与EGFR值正常(≥为90mL/min/1.73m2)相比，EGFR值为+lt；60mL/min/1.73m2(调整后优势比(OR)为2.02；95%可信区间[CI]为1.25~3.26)的患者死亡或致残的风险较高，而EGFR值为60~89mL/min/1.73m2的患者死亡或致残的概率无显著差异(OR为1.01；95%CI为0.70~1.46)。EGFR值为90、60~89和60mL/≥/1.73m2的患者死亡或残疾的OR值分别为0.89(95%CI，0.55~1.44)、1.13(0.68~1.89)和3.6(1.47~8.80)(交互作用P=0.02)。EGFR降低与脑出血后的不良结局相关。EGFR组和治疗分配之间具有统计学意义的相互作用引发了对肾损害患者强化降压治疗的安全性担忧。ClinicalTrials.gov标识符：NCT01176565。这项研究提供了II类证据，表明在自发性脑出血患者中，EGFR降低可以识别在加强血压控制后有死亡或残疾风险的患者。
The clinical effect of renal impairment on intracerebral hemorrhage (ICH) is unknown. This study sought to assess whether estimated glomerular filtration rate (eGFR) affects clinical outcomes or modifies the efficacy of intensive systolic blood pressure (BP) control (target, 110–139 mm Hg) against the standard (target, 140–179 mm Hg) among patients with ICH. We conducted post hoc analyses of ATACH-2, a randomized, 2-group, open-label trial. The baseline eGFR of each eligible patient was calculated using the Chronic Kidney Disease Epidemiology Collaboration equation. The outcome of interest was death or disability at 90 days. Multivariate logistic regression models were used for analysis. Among the 1,000 patients randomized, 974 were analyzed. The median baseline eGFR was 88 (interquartile range, 68, 99) mL/min/1.73 m2; 451 (46.3%), 363 (37.3%), and 160 (16.4%) patients had baseline eGFR values of ≥90, 60–89, and <60 mL/min/1.73 m2, respectively. Compared with normal eGFR (≥90 mL/min/1.73 m2), higher odds of death or disability were noted among those with eGFR values of <60 mL/min/1.73 m2 (adjusted odds ratio [OR], 2.02; 95% confidence interval [CI], 1.25–3.26) but not among those with eGFR values of 60–89 mL/min/1.73 m2 (OR, 1.01; 95% CI, 0.70–1.46). The odds of death or disability were significantly higher in the intensive arm among patients with decreased eGFR; the ORs were 0.89 (95% CI, 0.55–1.44), 1.13 (0.68–1.89), and 3.60 (1.47–8.80) in patients with eGFR values of ≥90, 60–89, and <60 mL/min/1.73 m2, respectively (p for interaction = 0.02). Decreased eGFR is associated with unfavorable outcomes following ICH. The statistically significant interaction between the eGFR group and treatment assignment raised safety concerns for the intensive BP-lowering therapy among patients with renal impairment. Clinicaltrials.gov identifier: NCT01176565. This study provides Class II evidence that in spontaneous ICH, decreased eGFR identifies patients at risk of death or disability following intensive BP control.