Abstract
BackgroundAcute Kidney Injury (AKI) is a frequent complication of severe SARS-CoV-2 infection. Multiple mechanisms are involved in COVID-19-associated AKI, from direct viral infection and secondary inflammation to complement activation and microthrombosis. However, data are limited in critically-ill patients. In this study, we sought to describe the prevalence, risk factors and prognostic impact of AKI in this setting.MethodsRetrospective monocenter study including adult patients with laboratory confirmed SARS-CoV-2 infection admitted to the ICU of our university Hospital. AKI was defined according to both urinary output and creatinine KDIGO criteria.ResultsOverall, 100 COVID-19 patients were admitted. AKI occurred in 81 patients (81%), including 44, 10 and 27 patients with AKI stage 1, 2 and 3 respectively. The severity of AKI was associated with mortality at day 28 (p = 0.013). Before adjustment, the third fraction of complement (C3), interleukin-6 (IL-6) and ferritin levels were higher in AKI patients. After adjustment for confounders, both severity (modified SOFA score per point) and AKI were associated with outcome. When forced in the final model, C3 (OR per log 0.25; 95% CI 0.01–4.66), IL-6 (OR per log 0.83; 95% CI 0.51–1.34), or ferritin (OR per log 1.63; 95% CI 0.84–3.32) were not associated with AKI and did not change the model.ConclusionIn conclusion, we did not find any association between complement activation or inflammatory markers and AKI. Proportion of patients with AKI during severe SARS-CoV-2 infection is higher than previously reported and associated with outcome.
Highlights
Acute Kidney Injury (AKI) is a frequent complication of severe SARS-CoV-2 infection but data are scarce in Intensive care unit (ICU)
Multiple mechanisms are involved in COVID-19-associated AKI, ranging from direct viral infection of the kidney and secondary inflammation to complement activation and microthrombosis [7]
Severe COVID-19 is associated with uncontrolled systemic inflammatory response with high levels of IL-6 [8] that could potentially lead to intrarenal inflammation and increased vascular permeability and share several features with hyperferritinemic syndromes such as Joseph et al Ann
Summary
Multiple mechanisms are involved in COVID-19-associated AKI, from direct viral infection and secondary inflammation to complement activation and microthrombosis. Since December 2019, severe acute respiratory coronavirus 2 (SARS-CoV-2) has spread worldwide, causing more than 6.6 million cases and 390 000 deaths [1] This pandemic has put unprecedented pressure on healthcare systems and especially on intensive care units (ICUs). Acute Kidney Injury (AKI) is a frequent complication of severe SARS-CoV-2 infection but data are scarce in ICUs. AKI has been previously reported with an average incidence of 11% (8–17%) overall, with highest ranges in Multiple mechanisms are involved in COVID-19-associated AKI, ranging from direct viral infection of the kidney and secondary inflammation to complement activation and microthrombosis [7]. Both IL-6 [11] and complement [12] have been proposed as therapeutic targets and understanding their role in COVID19-associated AKI is a priority
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