The kidney, COVID-19, and the chemokine network: an intriguing trio.
Gianluigi TavernaSimona Di FrancescoElena Monica BorroniDaniel YiuElena ToniatoSamantha MilanesiMaurizio Chiriva-InternatiRobert S BresalierMatteo ZanoniPaolo VotaDavide MaffeiMatteo JustichFabio GrizziPublished in: International urology and nephrology (2020)
On December 30th 2019, some patients with pneumonia of unknown etiology were reported in the Program for Monitoring Emerging Diseases (ProMED), a program run by the International Society for Infectious Diseases (ISID), hypothesized to be related to subjects who had had contact with the seafood market in Wuhan, China. Chinese authorities instituted an emergency agency aimed at identifying the source of infection and potential biological pathogens. It was subsequently named by the World Committee on Virus Classification as 2019-nCoV (2019-novel coronavirus) or severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). A number of studies have demonstrated that 2019-nCoV and the SARS-CoV shared the same cell entry receptor named angiotensin-converting enzyme 2 (ACE2). This is expressed in human tissues, not only in the respiratory epithelia, but also in the small intestines, heart, liver, and kidneys. Here, we examine the most recent findings on the effects of SARS-CoV-2 infection on kidney diseases, mainly acute kidney injury, and the potential role of the chemokine network.
Keyphrases
- respiratory syndrome coronavirus
- sars cov
- angiotensin converting enzyme
- coronavirus disease
- infectious diseases
- angiotensin ii
- acute kidney injury
- quality improvement
- endothelial cells
- machine learning
- heart failure
- emergency department
- gene expression
- deep learning
- cardiac surgery
- healthcare
- atrial fibrillation
- cell therapy
- stem cells
- induced pluripotent stem cells
- gram negative
- network analysis
- mesenchymal stem cells
- intensive care unit
- risk assessment
- climate change
- bone marrow