Autor: |
Ishan Paranjpe, Kumardeep Chaudhary, Kipp W Johnson, Suraj K Jaladanki, Shan Zhao, Jessica K De Freitas, Elisabet Pujdas, Fayzan Chaudhry, Erwin P Bottinger, Matthew A Levin, Zahi A Fayad, Alexander W Charney, Jane Houldsworth, Carlos Cordon-Cardo, Benjamin S Glicksberg, Girish N Nadkarni |
Jazyk: |
angličtina |
Rok vydání: |
2021 |
Předmět: |
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Zdroj: |
PLoS ONE, Vol 16, Iss 2, p e0247366 (2021) |
Druh dokumentu: |
article |
ISSN: |
1932-6203 |
DOI: |
10.1371/journal.pone.0247366 |
Popis: |
BackgroundSevere acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and the associated Coronavirus Disease 2019 (COVID-19) is a public health emergency. Acute kidney injury (AKI) is a common complication in hospitalized patients with COVID-19 although mechanisms underlying AKI are yet unclear. There may be a direct effect of SARS-CoV-2 virus on the kidney; however, there is currently no data linking SARS-CoV-2 viral load (VL) to AKI. We explored the association of SARS-CoV-2 VL at admission to AKI in a large diverse cohort of hospitalized patients with COVID-19.Methods and findingsWe included patients hospitalized between March 13th and May 19th, 2020 with SARS-CoV-2 in a large academic healthcare system in New York City (N = 1,049) with available VL at admission quantified by real-time RT-PCR. We extracted clinical and outcome data from our institutional electronic health records (EHRs). AKI was defined by KDIGO guidelines. We fit a Fine-Gray competing risks model (with death as a competing risk) using demographics, comorbidities, admission severity scores, and log10 transformed VL as covariates and generated adjusted hazard ratios (aHR) and 95% Confidence Intervals (CIs). VL was associated with an increased risk of AKI (aHR = 1.04, 95% CI: 1.01-1.08, p = 0.02) with a 4% increased hazard for each log10 VL change. Patients with a viral load in the top 50th percentile had an increased adjusted hazard of 1.27 (95% CI: 1.02-1.58, p = 0.03) for AKI as compared to those in the bottom 50th percentile.ConclusionsVL is weakly but significantly associated with in-hospital AKI after adjusting for confounders. This may indicate the role of VL in COVID-19 associated AKI. This data may inform future studies to discover the mechanistic basis of COVID-19 associated AKI. |
Databáze: |
Directory of Open Access Journals |
Externí odkaz: |
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