Acute kidney injury in patients with SARS-CoV-2 infection

  • PDF / 1,307,056 Bytes
  • 8 Pages / 595.276 x 790.866 pts Page_size
  • 95 Downloads / 185 Views

DOWNLOAD

REPORT


Open Access

RESEARCH

Acute kidney injury in patients with SARS‑CoV‑2 infection Adrien Joseph1, Lara Zafrani1,3*, Asma Mabrouki1, Elie Azoulay1,2 and Michael Darmon1,2

Abstract  Background:  Acute 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. Methods:  Retrospective 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. Results:  Overall, 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. Conclusion:  In 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. Keywords:  Acute kidney injury, COVID-19, Complement system proteins, Interleukin-6, Outcome, Intensive care units Background 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 *Correspondence: [email protected] 1 Service de médecine Intensive et de réanimation médicale, Hôpital Saint-Louis, Assistance-Publique Hôpitaux de Paris, Paris University, 1 avenue Claude Vellefaux, 75010 Paris, France Full list of author information is available at the end of the article

the critically ill (23%; 14–35%) [2–4]. Different applications of the Kidney Disease Improving Global Outcomes (KDIGO) criteria for AKI, in particular different methods to estimate missing baseline creatinine and handling urinary output, can cause important variations of estimated incidence [5, 6] and may contribute to the discrepancies among these studies