The Association of COVID-19 With Acute Kidney Injury Independent of Severity of Illness: A Multicenter Cohort Study.
The Association of COVID-19 With Acute Kidney Injury Independent of Severity of Illness: A Multicenter Cohort Study.
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DOI：
10.1053/j.ajkd.2020.12.007
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发表时间：
2021-04
期刊：
影响因子：
--
通讯作者：
Wilson FP
中科院分区：
文献类型：
--
作者：
Moledina DG;Simonov M;Yamamoto Y;Alausa J;Arora T;Biswas A;Cantley LG;Ghazi L;Greenberg JH;Hinchcliff M;Huang C;Mansour SG;Martin M;Peixoto A;Schulz W;Subair L;Testani JM;Ugwuowo U;Young P;Wilson FP
尽管冠状病毒病2019年(新冠肺炎)与急性肾脏损伤(AKI)有关，但这种联系是否独立于低血压、肾毒素暴露和炎症等传统风险因素尚不清楚。我们测试了新冠肺炎与AKI的独立关联性。多中心、观察性、队列研究。2020年3月10日至2020年8月31日期间，耶鲁纽黑文卫生系统内6家医院中的1家住院的患者，通过鼻咽样本的聚合酶链式反应进行了严重急性呼吸综合征冠状病毒2(SARS-CoV-2)检测。SARS-CoV-2检测呈阳性。AKI按KDIGO(肾脏疾病：改善全球预后)标准。使用时间更新的COX比例风险模型，在控制了入院时的不变因素(如人口学特征、合并症)和住院期间不断更新的时变因素(如生命体征、药物、实验室结果、呼吸衰竭)后，评估了新冠肺炎与急性心肌梗死的相关性。在22,122名住院患者中，2,600名SARS-CoV-2检测呈阳性，19,522名检测为阴性。与试验阴性的患者相比，新冠肺炎患者有更多的急性肾损伤(30.6%比18.2%；绝对风险差异12.5%[95%可信区间10.6%~14.3%])和需要透析的急性肾损伤(8.5%比3.6%)，而急性肾损伤的恢复率更低(58%比69.8%)。与无新冠肺炎的患者相比，新冠肺炎患者的炎症标志物(C-反应蛋白、铁蛋白)水平更高，血管加压药和利尿剂的使用量更多。单因素分析显示，与无新冠肺炎的患者相比，有新冠肺炎的患者急性心肌梗死的发生率更高(危险比，1.84[95%CI，1.73~1.95])。在一个完全调整了人口统计学变量、合并症、生命体征、药物和实验室结果的模型中，新冠肺炎仍然与急性心肌梗死的高发生率相关(调整后的风险比，1.40[95%可信区间，1.29-1.53])。残留混杂的可能性。新冠肺炎与急性心肌梗死的高发病率有关，但对已知风险因素的调整并未完全解释这一现象。这表明急性肾损伤的发生机制可能包括新冠肺炎对肾脏的直接影响或其他未被测量的介质。未来的研究应该评估新冠肺炎可能导致急性心肌梗死的独特途径。
Although coronavirus disease 2019 (COVID-19) has been associated with acute kidney injury (AKI), it is unclear whether this association is independent of traditional risk factors such as hypotension, nephrotoxin exposure, and inflammation. We tested the independent association of COVID-19 with AKI. Multicenter, observational, cohort study. Patients admitted to 1 of 6 hospitals within the Yale New Haven Health System between March 10, 2020, and August 31, 2020, with results for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) testing via polymerase chain reaction of a nasopharyngeal sample. Positive test for SARS-CoV-2. AKI by KDIGO (Kidney Disease: Improving Global Outcomes) criteria. Evaluated the association of COVID-19 with AKI after controlling for time-invariant factors at admission (eg, demographic characteristics, comorbidities) and time-varying factors updated continuously during hospitalization (eg, vital signs, medications, laboratory results, respiratory failure) using time-updated Cox proportional hazard models. Of the 22,122 patients hospitalized, 2,600 tested positive and 19,522 tested negative for SARS-CoV-2. Compared with patients who tested negative, patients with COVID-19 had more AKI (30.6% vs 18.2%; absolute risk difference, 12.5% [95% CI, 10.6%-14.3%]) and dialysis-requiring AKI (8.5% vs 3.6%) and lower rates of recovery from AKI (58% vs 69.8%). Compared with patients without COVID-19, patients with COVID-19 had higher inflammatory marker levels (C-reactive protein, ferritin) and greater use of vasopressors and diuretic agents. Compared with patients without COVID-19, patients with COVID-19 had a higher rate of AKI in univariable analysis (hazard ratio, 1.84 [95% CI, 1.73-1.95]). In a fully adjusted model controlling for demographic variables, comorbidities, vital signs, medications, and laboratory results, COVID-19 remained associated with a high rate of AKI (adjusted hazard ratio, 1.40 [95% CI, 1.29-1.53]). Possibility of residual confounding. COVID-19 is associated with high rates of AKI not fully explained by adjustment for known risk factors. This suggests the presence of mechanisms of AKI not accounted for in this analysis, which may include a direct effect of COVID-19 on the kidney or other unmeasured mediators. Future studies should evaluate the possible unique pathways by which COVID-19 may cause AKI.
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DOI：
10.1016/0021-9681(79)90012-2
发表时间：
1979-01-01
期刊：
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