• Dennis G Moledina, Michael Simonov, Yu Yamamoto, Jameel Alausa, Tanima Arora, Aditya Biswas, Lloyd G Cantley, Lama Ghazi, Jason H Greenberg, Monique Hinchcliff, Chenxi Huang, Sherry G Mansour, Melissa Martin, Aldo Peixoto, Wade Schulz, Labeebah Subair, Jeffrey M Testani, Ugochukwu Ugwuowo, Patrick Young, and F Perry Wilson.
• Section of Nephrology, Department of Internal Medicine, Yale School of Medicine, New Haven, CT; Clinical and Translational Research Accelerator, Department of Internal Medicine, Yale School of Medicine, New Haven, CT.
• Am. J. Kidney Dis. 2021 Apr 1; 77 (4): 490-499.e1.

Rationale & ObjectiveAlthough 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.Study DesignMulticenter, observational, cohort study.Setting & ParticipantsPatients 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.ExposurePositive test for SARS-CoV-2.OutcomeAKI by KDIGO (Kidney Disease: Improving Global Outcomes) criteria.Analytical ApproachEvaluated 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.ResultsOf 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]).LimitationsPossibility of residual confounding.ConclusionsCOVID-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.Copyright © 2021 National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved.

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