<b><i>Background:</i></b> Acute kidney injury (AKI) in patients with COVID-19 can be caused by multiple mechanisms. Renal resistive index (RRI) is a noninvasive instrument to evaluate kidney hemodynamics, and it is obtained by analysis of intrarenal arterial waves using Doppler ultrasound. This study aimed to determine the role of RRI in predicting AKI and adverse outcomes in critically ill patients with COVID-19. <b><i>Methods:</i></b> This cross-sectional study included 65 patients with confirmed SARS-CoV-2 pneumonia admitted to the critical care unit from April 1, 2020, to June 20, 2020. Informed consent was obtained from all individual participants included in the study. Cardiac, pulmonary, and kidney ultrasonographic evaluations were performed in a protocolized way. <b><i>Results:</i></b> In this cohort, 65 patients were included, mean age was 53.4 years, 79% were male, and 35% were diabetic. Thirty-four percent of patients developed AKI, 12% required RRT, and 35% died. Of the patients who developed AKI, 68% had RRI ≥ 0.7. Also, 75% of the patients who required RRT had RRI ≥ 0.7. In the adjusted Cox model, the RRI ≥ 0.7 was associated with higher mortality (HR 2.86, 95% CI: 1.19–6.82, <i>p</i> = 0.01). <b><i>Conclusions:</i></b> Critical care ultrasonography is a noninvasive, reproducible, and accurate bedside method that has proven its usefulness. An elevated RRI may have a role in predicting AKI, RRT initiation, and mortality in patients with severe SARS-CoV-2 pneumonia.

Water excretion in normal subjects during water loading was impaired after the administration of the short‐acting diuretics, mannitol, quinethazone, furosemide, and ethacrynic acid. Correlation between antidiuresis and body‐fluid‐volume depletion was established. Minimum contraction of body‐fluid volume is postulated as the cause of the antidiuresis. It is postulated that free water formation in the urine is regulated by several intra‐ and extrarenal factors; the role of the antidiuretic hormone is uncertain.

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