• James Watchorn, Dean Y Huang, Jennifer Joslin, Kate Bramham, and Sam D Hutchings.
• School of Immunology and Microbial Sciences, Faculty of Life Sciences and Medicine, King's College London, London, UK.
• Shock. 2021 Apr 1; 55 (4): 479487479-487.

BackgroundAcute kidney injury (AKI) is a common complication of COVID-19 critical illness but the pathophysiology is uncertain. Some evidence has indicated that a vascular aetiology may be implicated. We used contrast-enhanced ultrasound (CEUS) and echocardiography to study renal perfusion and global blood flow and compared our findings with measurements taken in a group of septic shock patients and healthy volunteers.MethodsProspective case-control study. Renal perfusion variables were assessed with CEUS; macrovascular blood flow was assessed using Doppler analysis of large renal vessels; echocardiography was used to assess right and left heart function and cardiac output.ResultsCEUS-derived parameters were reduced in COVID-19 associated AKI compared with healthy controls (perfusion index 3,415 vs. 548 a.u., P = 0·001; renal blood volume 7,794 vs. 3,338 a.u., P = 0·04). Renal arterial flow quantified using time averaged peak velocity was also reduced compared with healthy controls (36·6 cm/s vs. 20·9 cm/s, P = 0.004) despite cardiac index being similar between groups (2.8 L/min/m2 vs. 3.7 L/min/m2, P = 0.07). There were no differences in CEUS-derived or cardiac parameters between COVID-19 and septic shock patients but patients with septic shock had more heterogeneous perfusion variables.ConclusionBoth large and small vessel blood flow is reduced in patients with COVID-19 associated AKI compared with healthy controls, which does not appear to be a consequence of right or left heart dysfunction. A reno-vascular pathogenesis of COVID-19 AKI seems likely.Copyright © 2020 by the Shock Society.

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