L V K S Bhaskar1, Bijan Roshan2, Hamid Nasri3. 1. Department of Zoology, Guru Ghasidas Vishwavidyalaya, Bilaspur, India. 2. Division of Nephrology, Scripps Clinic, La Jolla, La Jolla, California, USA. 3. Department of Nephropathology, Nickan Research Institute, Isfahan, Iran, hamidnasri@med.mui.ac.ir.
Dear Editor,We appreciate the highly time-appropriate information presented in the article “Coronavirus Disease 19Infection Does Not Result in Acute Kidney Injury: An Analysis of 116 Hospitalized Patients from Wuhan, China” by Wang et al. [1]. COVID-19 (coronavirus disease) is a newly emerged pandemic caused by a novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). As a close relative of other epidemic coronaviruses (SARS and Middle East Respiratory Syndrome), SARS-CoV-2 is highly contagious and exhibits flu-like symptoms with pneumonic illness [1]. Although 85% of patients recover from infection without needing hospitalization, elderly people and people with another condition that compromises the immune system such as hypertension or diabetes appear to develop serious illness [1, 2]. Detection of viral RNA in urine and kidney tissue of SARS-CoV-2-infectedpatients indicates the kidney as a target of infection [2]. Several of the recent reviews have mentioned kidney manifestations of COVID-19 [3, 4]. While angiotensin-converting enzyme 2 (ACE2) receptors are the functional receptor for the SARS coronavirus, their presentation in the lower respiratory tract, kidney, duodenum, and small intestine might provide possible routes of entry for the SARS-CoV [5]. Studies in a mouse model of SARS-CoV infection demonstrated that ACE2 expression is vital for viral entry and ACE2 overexpression is directly proportional to disease severity [6]. As bradykinin B1 receptor mediates the cross talk between ACE2 and the kinin-kallikrein system in setting the inflammation, selective bradykinin B1 receptor blockers could be used as a promising agent to prevent tissue inflammation during COVID-19 infection [7].Significant functional impairment of the kidney in COVID-19patients [8, 9] is well known, and we see that in our patients frequently. Development of acute kidney injury (AKI) is also associated with significant increased mortality during hospital stay [9]. AKI can be a surrogate for multi-organ failure and serves as a negative prognostic factor for survival in COVID-19patients [10].We wonder whether the incidence of AKI by reporting time, and not the total incidence of AKI, was reported in this study by Wang et al. [1] They report that as of February 13, 2020, 7 (6.03%) acute respiratory distress syndromepatients transferred to ICU died of respiratory failure. This is much lower than the overall mortality of more than 52% reported for acute respiratory distress syndrome in COVID-19patients from Wuhan [10]. We suspect the same methodologic problem underlies the underestimation of AKI in COVID-19 in his study. Therefore, larger studies in this regard are necessary.
Disclosure Statement
The authors report no conflict of interests.
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There was no financial support.
Author Contributions
Primary draft by L.V.K.S.B. B.R. edited the paper. H.N. conducted further edits. All authors read and signed the final paper.