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

• DOI: 10.1371/journal.pone.0247366
• Publication Date: 2021-02-24T18:41:34Z
• Authors: Ishan Paranjpe; Kumardeep Chaudhary; Kipp W. Johnson; Suraj K. Jaladanki; Shan Zhao; Jessica K. De Fre...; Elisabet Pujdas; Fayzan Chaudhry; Erwin P. Bottinger; Matthew A. Levin; Zahi A. Fayad; Alexander W. Charney; Jane Houldsworth; Carlos Cordon-Cardo; Benjamin S. Glick...; Girish N. Nadkarni
• Keywords: Adult; Male; Science; Comorbidity; Cohort Studies; 03 medical and health sciences; 0302 clinical medicine; Risk Factors; Humans; Hospital Mortality; Aged; Proportional Hazards Models; Retrospective Studies; Aged, 80 and over; SARS-CoV-2; Q; R; COVID-19; Acute Kidney Injury; Middle Aged; Viral Load; 3. Good health; Hospitalization; Medicine; Female; New York City; Research Article

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.