From the, Department of Acute Medicine, University College Hospital, Bloomsbury, London, UK.
Chair and Department of Experimental and Clinical Physiology, Laboratory of Centre for Preclinical Research, Medical University of Warsaw, Warszawa, Poland.
J Intern Med. 2021 May;289(5):688-699. doi: 10.1111/joim.13202. Epub 2020 Dec 6.
COVID-19 is caused by the coronavirus SARS-CoV-2, which uses angiotensin-converting enzyme 2 (ACE-2) as a receptor for cellular entry. It is theorized that ACE inhibitors (ACE-Is) or angiotensin receptor blockers (ARBs) may increase vulnerability to SARS-CoV-2 by upregulating ACE-2 expression, but ACE-I/ARB discontinuation is associated with clinical deterioration.
To determine whether ACE-I and ARB use is associated with acute kidney injury (AKI), macrovascular thrombosis and in-hospital mortality.
A retrospective, single-centre study of 558 hospital inpatients with confirmed COVID-19 admitted from 1 March to 30 April 2020, followed up until 24 May 2020. AKI and macrovascular thrombosis were primary end-points, and in-hospital mortality was a secondary end-point.
AKI occurred in 126 (23.1%) patients, 34 (6.1%) developed macrovascular thrombi, and 200 (35.9%) died. Overlap propensity score-weighted analysis showed no significant effect of ACE-I/ARB use on the risk of occurrence of the specified end-points. On exploratory analysis, severe chronic kidney disease (CKD) increases odds of macrovascular thrombi (OR: 8.237, 95% CI: 1.689-40.181, P = 0.009). The risk of AKI increased with advancing age (OR: 1.028, 95% CI: 1.011-1.044, P = 0.001) and diabetes (OR: 1.675, 95% CI: 1.065-2.633, P = 0.025). Immunosuppression was associated with lower risk of AKI (OR: 0.160, 95% CI: 0.029-0.886, P = 0.036). Advancing age, dependence on care, male gender and eGFR < 60 mL min /1.73 m increased odds of in-hospital mortality.
We did not identify an association between ACE-I/ARB use and AKI, macrovascular thrombi or mortality. This supports the recommendations of the European and American Societies of Cardiology that ACE-Is and ARBs should not be discontinued during the COVID-19 pandemic.
COVID-19 是由冠状病毒 SARS-CoV-2 引起的，该病毒使用血管紧张素转换酶 2（ACE-2）作为细胞进入的受体。理论上，血管紧张素转换酶抑制剂（ACE-Is）或血管紧张素受体阻滞剂（ARBs）可能通过上调 ACE-2 表达而增加对 SARS-CoV-2 的易感性，但 ACE-I/ARB 停药与临床恶化有关。
确定 ACE-I 和 ARB 使用是否与急性肾损伤（AKI）、大血管血栓形成和住院死亡率相关。
这是一项回顾性、单中心研究，纳入了 2020 年 3 月 1 日至 4 月 30 日期间确诊为 COVID-19 并住院的 558 名患者，随访至 2020 年 5 月 24 日。AKI 和大血管血栓形成是主要终点，住院死亡率是次要终点。
126 例（23.1%）患者发生 AKI，34 例（6.1%）发生大血管血栓形成，200 例（35.9%）死亡。重叠倾向评分加权分析显示，ACE-I/ARB 使用对特定终点的发生风险无显著影响。探索性分析显示，严重慢性肾脏病（CKD）增加大血管血栓形成的几率（OR：8.237，95%CI：1.689-40.181，P=0.009）。AKI 的风险随年龄增长而增加（OR：1.028，95%CI：1.011-1.044，P=0.001）和糖尿病（OR：1.675，95%CI：1.065-2.633，P=0.025）。免疫抑制与 AKI 的风险降低相关（OR：0.160，95%CI：0.029-0.886，P=0.036）。年龄增长、依赖护理、男性和 eGFR<60 mL/min/1.73 m2 增加了住院死亡率的几率。
我们没有发现 ACE-I/ARB 使用与 AKI、大血管血栓形成或死亡率之间存在关联。这支持了欧洲和美国心脏病学会的建议，即在 COVID-19 大流行期间不应停止使用 ACE-Is 和 ARBs。
