Open AccessAssociation 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 Jaladanki,
Shan Zhao,
Jessica K De Freitas,
Elisabet Pujdas,
Fayzan Chaudhry,
Erwin P. Böttinger,
Matthew A. Levin,
Zahi A. Fayad,
Alexander Charney,
Jane Houldsworth,
Carlos Cordón-Cardó,
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 , kidney disease , proportional hazards model , 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.