Division of General Internal and Emergency Medicine, Diabetes, and Metabolism.
Division of Endocrinology, Diabetes, and Metabolism.
Eur J Endocrinol. 2021 Apr;184(4):543-552. doi: 10.1530/EJE-20-1445.
While evidence on the interface between severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and the renin-angiotensin-aldosterone-system (RAAS) is accumulating, clinical data on RAAS peptide alteration among coronavirus disease-19 (COVID-19) patients is missing.
In this exploratory study, we prospectively included adult patients (aged ≥ 18 years) admitted between February 26 and April 30, 2020 to a tertiary care hospital in Switzerland. We assessed the association of an underlying SARS-CoV-2 infection and equilibrium serum levels of RAAS peptides in hospitalized COVID-19 patients 1:1 propensity-score matched with patients suffering from SARS-CoV-2-negative respiratory infections. Subgroup analyses involved stratification for taking RAAS inhibitors.
COVID-19 patients had about 50% lower equilibrium serum RAAS peptide levels as compared with matched controls (angiotensin I: 31.6 vs 66.8 pmol/L, -52.7% (95%CI: -68.5% to -36.9%); angiotensin II: 37.7 vs 92.5 pmol/L, -59.2% (95%CI: -72.1% to -46.3%); angiotensin (1-5): 3.3 vs 6.6 pmol/L, -49.7% (95%CI: -59.2% to -40.2%); angiotensin (1-7): 4.8 vs 7.6 pmol/L, -64.9% (95%CI: -84.5% to -45.3%)). While the plasma renin activity was lower in COVID-19 patients (88.6 vs 207.9 pmol/L, -58.5% (95%CI: -71.4% to -45.6%)), there was no difference of angiotensin-converting enzyme (ACE) and ACE2 plasma activity between the groups. Subgroup analyses revealed a pronounced RAAS peptide profile depression in COVID-19 patients among those not on RAAS inhibitors.
As compared with SARS-CoV-2-negative patients, we found a downregulated RAAS in presence of a SARS-CoV-2 infection. Whether the lower levels of the protective angiotensin (1-5) and (1-7) are linked to adverse outcomes in COVID-19 warrants further investigation.
虽然关于严重急性呼吸综合征冠状病毒 2（SARS-CoV-2）感染与肾素-血管紧张素-醛固酮系统（RAAS）之间的界面的证据正在不断增加，但关于 COVID-19 患者 RAAS 肽改变的临床数据仍缺乏。
在这项探索性研究中，我们前瞻性地纳入了 2020 年 2 月 26 日至 4 月 30 日期间入住瑞士一家三级护理医院的成年患者（年龄≥18 岁）。我们评估了 SARS-CoV-2 感染与住院 COVID-19 患者 RAAS 肽平衡血清水平之间的关联，这些患者与 SARS-CoV-2 阴性呼吸道感染的患者按 1:1 倾向评分匹配。亚组分析涉及分层服用 RAAS 抑制剂的情况。
COVID-19 患者的平衡血清 RAAS 肽水平比匹配对照低约 50%（血管紧张素 I：31.6 与 66.8 pmol/L，-52.7%（95%CI：-68.5%至-36.9%）；血管紧张素 II：37.7 与 92.5 pmol/L，-59.2%（95%CI：-72.1%至-46.3%）；血管紧张素（1-5）：3.3 与 6.6 pmol/L，-49.7%（95%CI：-59.2%至-40.2%）；血管紧张素（1-7）：4.8 与 7.6 pmol/L，-64.9%（95%CI：-84.5%至-45.3%））。虽然 COVID-19 患者的血浆肾素活性较低（88.6 与 207.9 pmol/L，-58.5%（95%CI：-71.4%至-45.6%）），但两组之间的血管紧张素转换酶（ACE）和 ACE2 血浆活性无差异。亚组分析显示，在未服用 RAAS 抑制剂的 COVID-19 患者中，RAAS 肽谱明显下降。在 SARS-CoV-2 感染存在的情况下，RAAS 的下调是否与 COVID-19 的不良结局有关，这仍需要进一步研究。
