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PLoS One . Association of SARS-CoV-2 viral load at admission with in-hospital acute kidney injury: A retrospective cohort study

tetano

Editor, Senior Moderator
PLoS One


. 2021 Feb 24;16(2):e0247366.
doi: 10.1371/journal.pone.0247366. eCollection 2021.
Association of SARS-CoV-2 viral load at admission with in-hospital acute kidney injury: A retrospective cohort study


Ishan Paranjpe[SUP] 1 2 [/SUP], Kumardeep Chaudhary[SUP] 3 4 [/SUP], Kipp W Johnson[SUP] 1 2 3 [/SUP], Suraj K Jaladanki[SUP] 1 2 [/SUP], Shan Zhao[SUP] 1 5 [/SUP], Jessica K De Freitas[SUP] 1 2 [/SUP], Elisabet Pujdas[SUP] 6 [/SUP], Fayzan Chaudhry[SUP] 1 2 [/SUP], Erwin P Bottinger[SUP] 2 [/SUP], Matthew A Levin[SUP] 1 5 [/SUP], Zahi A Fayad[SUP] 1 7 8 [/SUP], Alexander W Charney[SUP] 1 3 9 [/SUP], Jane Houldsworth[SUP] 6 [/SUP], Carlos Cordon-Cardo[SUP] 1 4 [/SUP], Benjamin S Glicksberg[SUP] 1 2 3 [/SUP], Girish N Nadkarni[SUP] 1 2 10 [/SUP]



Affiliations

Abstract

Background: Severe 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 findings: We 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.
Conclusions: VL 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.
 
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