• Muriel Ghosn, Nizar Attallah, Mohamed Badr, Khaled Abdallah, Bruno De Oliveira, Ashraf Nadeem, Yeldho Varghese, Dnyaseshwar Munde, Shameen Salam, Baraa Abduljawad, Khaled Saleh, Hussam Elkambergy, Ali Wahla, Ahmed Taha, Jamil Dibu, Ahmed Bayrlee, Fadi Hamed, Nadeem Rahman, and Jihad Mallat.
• Medical Sub-Specialties Institute, Department of Nephrology, Cleveland Clinic Abu Dhabi, Abu Dhabi 112412, United Arab Emirates.
• J Clin Med. 2021 Mar 15; 10 (6).

BackgroundCritically ill patients with COVID-19 are prone to develop severe acute kidney injury (AKI), defined as KDIGO (Kidney Disease Improving Global Outcomes) stages 2 or 3. However, data are limited in these patients. We aimed to report the incidence, risk factors, and prognostic impact of severe AKI in critically ill patients with COVID-19 admitted to the intensive care unit (ICU) for acute respiratory failure.MethodsA retrospective monocenter study including adult patients with laboratory-confirmed severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection admitted to the ICU for acute respiratory failure. The primary outcome was to identify the incidence and risk factors associated with severe AKI (KDIGO stages 2 or 3).ResultsOverall, 110 COVID-19 patients were admitted. Among them, 77 (70%) required invasive mechanical ventilation (IMV), 66 (60%) received vasopressor support, and 9 (8.2%) needed extracorporeal membrane oxygenation (ECMO). Severe AKI occurred in 50 patients (45.4%). In multivariable logistic regression analysis, severe AKI was independently associated with age (odds ratio (OR) = 1.08 (95% CI (confidence interval): 1.03-1.14), p = 0.003), IMV (OR = 33.44 (95% CI: 2.20-507.77), p = 0.011), creatinine level on admission (OR = 1.04 (95% CI: 1.008-1.065), p = 0.012), and ECMO (OR = 11.42 (95% CI: 1.95-66.70), p = 0.007). Inflammatory (interleukin-6, C-reactive protein, and ferritin) or thrombotic (D-dimer and fibrinogen) markers were not associated with severe AKI after adjustment for potential confounders. Severe AKI was independently associated with hospital mortality (OR = 29.73 (95% CI: 4.10-215.77), p = 0.001) and longer hospital length of stay (subhazard ratio = 0.26 (95% CI: 0.14-0.51), p < 0.001). At the time of hospital discharge, 74.1% of patients with severe AKI who were discharged alive from the hospital recovered normal or baseline renal function.ConclusionSevere AKI was common in critically ill patients with COVID-19 and was not associated with inflammatory or thrombotic markers. Severe AKI was an independent risk factor of hospital mortality and hospital length of stay, and it should be rapidly recognized during SARS-CoV-2 infection.

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