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Association of SARS-CoV-2 viral load at admission with in-hospital acute kidney injury: A retrospective cohort study
Author(s) -
Ishan Paranjpe,
Kumardeep Chaudhary,
Kipp W. Johnson,
Suraj K. Jaladanki,
Shan Zhao,
Jessica K. De Freitas,
Elisabet Pujdas,
Fayzan Chaudhry,
Erwin P. Böttinger,
Matthew A. Levin,
Zahi A. Fayad,
Alexander W. Charney,
Jane Houldsworth,
Carlos CordonCardo,
Benjamin S. Glicksberg,
Girish N. Nadkarni
Publication year - 2021
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0247366
Subject(s) - medicine , hazard ratio , acute kidney injury , retrospective cohort study , viral load , cohort , confidence interval , emergency department , cohort study , proportional hazards model , kidney disease , emergency medicine , immunology , virus , psychiatry
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 13 th and May 19 th , 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 log 10 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 log 10 VL change. Patients with a viral load in the top 50 th 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 50 th 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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