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Background Acute kidney injury (AKI) is common among patients hospitalised with COVID-19 and associated with worse prognosis. The aim of this study was to investigate the epidemiology, risk factors and outcomes of AKI in patients with COVID-19 in a large UK tertiary centre. Methods We analysed data of consecutive adults admitted with a laboratory-confirmed diagnosis of COVID-19 across two sites of a hospital in London, UK, from 1st January to 13th May 2020. Results Of the 1248 inpatients included, 487 (39%) experienced AKI (51% stage 1, 13% stage 2, and 36% stage 3). The weekly AKI incidence rate gradually increased to peak at week 5 (3.12 cases/100 patient-days), before reducing to its nadir (0.83 cases/100 patient-days) at the end the study period (week 10). Among AKI survivors, 84.0% had recovered renal function to pre-admission levels before discharge and none required on-going renal replacement therapy (RRT). Pre-existing renal impairment [odds ratio (OR) 3.05, 95%CI 2.24–4,18; p <  0.0001], and inpatient diuretic use (OR 1.79, 95%CI 1.27–2.53; p <  0.005) were independently associated with a higher risk for AKI. AKI was a strong predictor of 30-day mortality with an increasing risk across AKI stages [adjusted hazard ratio (HR) 1.59 (95%CI 1.19–2.13) for stage 1; p < 0.005, 2.71(95%CI 1.82–4.05); p < 0.001for stage 2 and 2.99 (95%CI 2.17–4.11); p < 0.001for stage 3]. One third of AKI3 survivors (30.7%), had newly established renal impairment at 3 to 6 months. Conclusions This large UK cohort demonstrated a high AKI incidence and was associated with increased mortality even at stage 1. Inpatient diuretic use was linked to a higher AKI risk. One third of survivors with AKI3 exhibited newly established renal impairment already at 3–6 months.

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Background: Acute 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 contrastenhanced 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. Methods: Prospective casecontrol 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. Results: CEUS-derived parameters were reduced in COVID-19 associated AKI compared with healthy controls (perfusion index 3,415 vs. 548 a.u., P ¼ 0Á001; renal blood volume 7,794 vs. 3,338 a.u., P ¼ 0Á04). Renal arterial flow quantified using time averaged peak velocity was also reduced compared with healthy controls (36Á6 cm/s vs. 20Á9 cm/s, P ¼ 0.004) despite cardiac index being similar between groups (2.8 L/min/m 2 vs. 3.7 L/min/m 2 , P ¼ 0.07). There were no differences in CEUSderived or cardiac parameters between COVID-19 and septic shock patients but patients with septic shock had more heterogeneous perfusion variables. Conclusion: Both 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.