The experiences of UK-Chinese individuals during the COVID-19 pandemic: A qualitative interview study.

Infectious disease outbreaks have historically been associated with stigmatisation towards minority groups, specifically those associated with the geographical region that the disease was first identified. We aimed to investigate how the emerging COVID-19 pandemic was experienced by UK-resident individuals of Chinese ethnicity: how their perceived cultural and ethnic identity influenced their experiences, and how early insights into the pandemic in China influenced attitudes and behaviours. We undertook in-depth semi-structured interviews with individuals who self-identified as UK-Chinese. Participants were recruited from three cities in the UK. Interviews were undertaken over the telephone between 9th April 2020 and 16th July 2020. Interviews were digitally recorded and transcribed verbatim. Transcripts were coded using NVivo software and analysed using inductive thematic analysis. Sixteen individuals were interviewed. Three main themes were identified: (1) Attribution of stigma, (2) Pandemic legacies, and (3) Individual versus societal responses. These reflected six sub-themes: (1) Stigmatisation through (mis)identity, (2) Markers of pandemic awareness, (3) Legacies of previous pandemics, (4) Ascription of blame, (5) Extent of freedom, and (6) Implicit faith in government. Experiences of xenophobia included accounts of physical violence. UK-Chinese individuals experienced and perceived widespread xenophobia, in the context of media representations that ascribed blame and exacerbated stigmatisation. Prior experience of respiratory epidemics, and insight into the governmental and societal response in China, contributed to the early adoption of face masks. This in turn marked UK-Chinese individuals as targets for abuse. Awareness is needed to safeguard stigmatized groups from social and economic harm in future infectious disease pandemics.

A survey on acute kidney injury in severely and critically ill COVID-19 patients without chronic kidney disease.

BACKGROUND: Research has shown that acute kidney injury (AKI) has a noticeable incidence in critically ill patients with coronavirus disease 2019 (COVID-19). Patients with prior renal insufficiency are particularly susceptible to severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), due to their immune dysfunction. However, most patients with COVID-19 do not have a history of kidney dysfunction, and few studies have focused on the incidence of AKI among COVID-19 patients without chronic kidney disease (CKD). In this study, we aimed to investigate the occurrence of AKI in severely and critically ill COVID-19 patients, with a particular focus on those without a CKD history. METHODS: A single-center retrospective study of 96 patients with COVID-19 in China between February 7 and March 3, 2020 was conducted. All patients were diagnosed by nucleic acid test (NAT) for SARS-CoV-2. Enrolled patients were divided into the severely or critically ill group according to the defined criteria. Patients' epidemiological, clinical, and laboratory characteristics, along with their treatment information, were collected from the medical history system. The occurrence of AKI was compared between the severe and critical patients, and between patients with or without a history of CKD. The diagnostic criteria for AKI included an increase in the serum creatinine level to ≥1.5-fold the level at baseline within 7 days according to the Kidney Disease: Improving Global Outcomes (KDIGO) guidelines. Renal outcomes were defined as AKI or non-AKI. RESULTS: Four patients (4.2%) developed AKI, all of whom were in the critically ill group, and 3 (75%) of whom died. Out of the 90 severely and critically ill COVID-19 patients without CKD, 3 (3.3%) patients developed AKI; out of the 6 patients with CKD, 1 (16.7%) patient developed AKI. Age, disease severity, procalcitonin, C-reactive protein, and interleukin-6 were correlated with AKI onset in severely and critically ill COVID-19 patients, while lymphocyte count and estimated glomerular filtration rate at admission were inversely related to the development of AKI. CONCLUSIONS: Only 3.3% of severely and critically ill COVID-19 patients without CKD in our research cohort developed AKI. Critically ill patients may be more susceptible to AKI than severely ill patients.

Single-cell analysis of angiotensin-converting enzyme II expression in human kidneys and bladders reveals a potential route of 2019 novel coronavirus infection.

BACKGROUND: Since 2019, a novel coronavirus named 2019 novel coronavirus (2019-nCoV) has emerged worldwide. Apart from fever and respiratory complications, acute kidney injury has been observed in a few patients with coronavirus disease 2019. Furthermore, according to recent findings, the virus has been detected in urine. Angiotensin-converting enzyme II (ACE2) has been proposed to serve as the receptor for the entry of 2019-nCoV, which is the same as that for the severe acute respiratory syndrome. This study aimed to investigate the possible cause of kidney damage and the potential route of 2019-nCoV infection in the urinary system. METHODS: We used both published kidney and bladder cell atlas data and new independent kidney single-cell RNA sequencing data generated in-house to evaluate ACE2 gene expression in all cell types in healthy kidneys and bladders. The Pearson correlation coefficients between ACE2 and all other genes were first generated. Then, genes with r values larger than 0.1 and P values smaller than 0.01 were deemed significant co-expression genes with ACE2. RESULTS: Our results showed the enriched expression of ACE2 in all subtypes of proximal tubule (PT) cells of the kidney. ACE2 expression was found in 5.12%, 5.80%, and 14.38% of the proximal convoluted tubule cells, PT cells, and proximal straight tubule cells, respectively, in three published kidney cell atlas datasets. In addition, ACE2 expression was also confirmed in 12.05%, 6.80%, and 10.20% of cells of the proximal convoluted tubule, PT, and proximal straight tubule, respectively, in our own two healthy kidney samples. For the analysis of public data from three bladder samples, ACE2 expression was low but detectable in bladder epithelial cells. Only 0.25% and 1.28% of intermediate cells and umbrella cells, respectively, had ACE2 expression. CONCLUSION: This study has provided bioinformatics evidence of the potential route of 2019-nCoV infection in the urinary system.