Impact of dexamethasone use to prevent from severe COVID-19-induced acute kidney injury

© The Author(s) 2021. Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http:// creat iveco mmons. org/ licen ses/ by/4. 0/. The Creative Commons Public Domain Dedication waiver (http:// creat iveco mmons. org/ publi cdoma in/ zero/1. 0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data. To the editor Since the first wave of COVID-19, the management of patients with severe COVID-19 in intensive care unit (ICU) has changed with the widespread use of dexamethasone (DXM) in severe patients [1]. Indeed, RECOVERY trial [2] showed a decrease in both mortality at day 28 and the number of patients who received renal replacement therapy (RRT) with DXM. We have previously reported a higher than usual incidence of acute kidney injury (AKI) (80%) in severe COVID-19 patients treated in ICU [3]. Like lung injury, specific SARS-CoV-2 inflammatory process was previously suggested in AKI pathogenesis [4, 5] and is susceptible to be improved by DXM. Besides, in another report, we recently described a 15% incidence of chronic kidney disease (CKD) at 3 months after COVID19-induced AKI [6], all of these patients developing acute kidney disease (AKD) before CKD. The aim of this report was to assess the independent clinical effect of DXM on the prevention of severe COVID-19-induced AKI. We carried out a prospective study in the medical ICU of the University Hospital of Bordeaux (France) from March 17, 2020, to December 20, 2020. All patients admitted for a severe COVID-19 were included. DXM was exclusively used during the second wave starting in Bordeaux (France) on August 6 at 6 mg per day for 10 days at ICU admission. Patients who presented AKI at ICU admission were excluded from the analysis.


To the editor
Since the first wave of COVID-19, the management of patients with severe COVID-19 in intensive care unit (ICU) has changed with the widespread use of dexamethasone (DXM) in severe patients [1]. Indeed, RECOVERY trial [2] showed a decrease in both mortality at day 28 and the number of patients who received renal replacement therapy (RRT) with DXM. We have previously reported a higher than usual incidence of acute kidney injury (AKI) (80%) in severe COVID-19 patients treated in ICU [3]. Like lung injury, specific SARS-CoV-2 inflammatory process was previously suggested in AKI pathogenesis [4,5] and is susceptible to be improved by DXM. Besides, in another report, we recently described a 15% incidence of chronic kidney disease (CKD) at 3 months after COVID-19-induced AKI [6], all of these patients developing acute kidney disease (AKD) before CKD. The aim of this report was to assess the independent clinical effect of DXM on the prevention of severe COVID-19-induced AKI.
We carried out a prospective study in the medical ICU of the University Hospital of Bordeaux (France) from March 17, 2020, to December 20, 2020. All patients admitted for a severe COVID-19 were included. DXM was exclusively used during the second wave starting in Bordeaux (France) on August 6 at 6 mg per day for 10 days at ICU admission. Patients who presented AKI at ICU admission were excluded from the analysis. (Table 1) From March 17, 2020, 126 patients were admitted in our unit, 26/126 patients (21%) were excluded because of AKI at ICU admission (5 and 21 patients, in first and second waves, respectively). DXM was used in all patients in the second wave and in none of the first wave. In the 100 patients included, median age was 63 ± 11 years, 59/100 (59%) had hypertension, 10/100 (10%) suffered from CKD and 48/100 (48%) required mechanical ventilation (MV) in the first 24 h. In the study population, 56/100 (56%) patients developed AKI: 39/52 (75%) and 17/48 (35%) patients (p < 0.001), in the first and second waves, respectively. AKD was observed in 24/100 (24%) of patients: 14/52 (27%) patients in the first wave and 10/48 (21%) in the second wave (p = 0.49). In univariate analysis, the use of DXM ( Our study suggests an independent effect of DXM to prevent from AKI in severe COVID-19 patients. This result needs to be confirmed in larger studies.

Patients characteristics
High rate of vasopressors and greater intravenous fluid therapy reported during the first wave imaged the earlier and more frequent use of MV, without reflecting the patients' severity admitted in our ICU. Indeed, patients admitted during the second wave had more comorbidities and were older, which explains the increased mortality trend observed in our study.
Lack of effect of DXM on RRT in our study can be explained by a lack of power and by the too weak effect of corticosteroids on AKI.
Our results could indicate an important impact of inflammatory state in the pathogenesis of COVID-19-induced AKI. These results support the hypothesis that corticosteroid therapy can reduce "inflammatory" AKI incidence (specific of COVID-19 infection) but has no impact on "maladaptive repair" lesions secondary to AKI that can lead to an AKD.

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