Abstract

Hemodialysis patients (HD) are expected to have excess mortality in coronavirus disease 2019 (COVID-19). This was challenged by a recent study reporting HD patients to have comparable mortality and less ICU admissions when hospitalized with COVID-19. An altered immune system due to chronic inflammation might protect HD-patients from severe COVID-19. Therefore, we aimed to describe the peripheral blood immune phenotype in HD-patients and respective controls with COVID-19.MethodsSixty-four patients (31 HD, 33 non-HD) with PCR-confirmed COVID-19 and 16 control patients (10 HD, 6 non-HD) were prospectively included. According to symptoms, COVID-19 patients were categorized as asymptomatic/mild, moderate or severe COVID-19 phenotypes. Cytokine profiling and immune phenotyping was performed.ResultsTh1 and Th17 plasma cytokine levels were highly increased in HD patients without COVID-19 and were not significantly regulated during COVID-19. In non-HD COVID-19 patients these cytokines increased significantly with disease severity. While all patients with moderate or severe COVID-19 showed hallmarks of COVID-19 such as decreased CD3+, CD4+ and CD8+ and CD4+CD25hiFoxP3+ regulatory T cells, significantly increased CD38+CD8+ effector memory and CD38+CD8+ TEMRA T cells were detected in moderate/severe COVID-19 HD patients, which was not observed in non-HD patients with moderate or severe COVID-19. Furthermore, CD161+CD8+ T cells decreased significantly in non-HD COVID-19 patients dependent on disease severity, but not in HD patients. Dynamics of B cells and subtypes were comparable in HD and non-HD COVID-19 patients.ConclusionsHD patients might be protected from severe COVID-19 due to their chronic inflammatory state with increased CD38+CD8+ effector memory and TEMRA T cells as well as CD161+CD8+ T cells.

Highlights

  • HD patients might be protected from severe COVID-19 due to their chronic inflammatory state with increased CD38+CD8+ effector memory and TEMRA T cells as well as CD161+CD8+ T cells

  • The coronavirus disease 2019 (COVID-19) pandemic induced by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a world-wide crisis and has increased mortality in patients with underlying chronic diseases such as diabetes, obesity, coronary heart disease, hypertension and chronic kidney disease (CKD) [1]

  • The non-HD patients, who suffered from asymptomatic/mild COVID-19 were health-care workers routinely screened at our hospital and tested positive for SARS-CoV2

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Summary

Introduction

The coronavirus disease 2019 (COVID-19) pandemic induced by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a world-wide crisis and has increased mortality in patients with underlying chronic diseases such as diabetes, obesity, coronary heart disease, hypertension and chronic kidney disease (CKD) [1]. There are two register analyses from the US and one from the ERA-EDTA showing a mortality rate in HD-patients ranging between 20 to 31%, respectively [4, 5]. These data have been challenged by a recent retrospective cohort study comparing patients with HDtherapy hospitalized due to COVID-19, who were propensity matched to patients without kidney failure [6]. They reported significantly decreased in-hospital mortality rates of 10%, which did not differ from patients without HD. There have been various speculations that uremia might chronically tamper the immune system and might protect patients from hyperinflammation and cytokine storm that is supposed to lead to pulmonary failure in COVID-19

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