Abstract
Since the outbreak of Coronavirus Disease 2019 (COVID-19) in Wuhan, China, in December of 2019, it has rapidly become a global pandemic. Although acute respiratory disorder is the main manifestation of COVID-19, acute kidney injury (AKI) is another important extrapulmonary complication, which has a critical impact on the prognosis and mortality of patients. Current understanding about the exact pathogenesis of AKI in COVID-19 is unclear. Several studies have suggested that intrarenal, pre-renal and post-renal factors mediated collaboratively by direct virus attack, overloaded immune responses, drugs, sepsis, coagulation dysfunction, and underlying diseases may all be involved in the pathogenesis of AKI. This article reviews the current understanding of the pathogenesis of AKI in COVID-19.
Highlights
The rapid outbreak of COVID-19 caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that emerged in Wuhan, China, in December of 2019, has rapidly become a potentially life-threatening and economically destructive global pandemic
Peng et al (2020) detected viral RNA of SARS-CoV-2 from the urine of COVID-19 patients, even in those without urinary symptoms. This confirmed that SARS-CoV-2 can invade the urinary system and enter the urine through glomerular filtration. These studies suggested that SARS-CoV-2 can directly infect the kidney to induce acute kidney injury (AKI)
In the kidney injury model mediated by nephrotoxicity, IL-6 correlates with the onset and severity of AKI and aggregate renal injury by recruiting neutrophils (Nechemia-Arbely et al, 2008)
Summary
The rapid outbreak of COVID-19 caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that emerged in Wuhan, China, in December of 2019, has rapidly become a potentially life-threatening and economically destructive global pandemic. Recent clinical studies and autopsies have provided more evidence that SARS-CoV-2 can directly infect the kidney. Peng et al (2020) detected viral RNA of SARS-CoV-2 from the urine of COVID-19 patients, even in those without urinary symptoms. This confirmed that SARS-CoV-2 can invade the urinary system and enter the urine through glomerular filtration To conclude, these studies suggested that SARS-CoV-2 can directly infect the kidney to induce AKI. The viral-cell membrane fusion is critical during the attack, which indicates that specific proteolytic cleavage of the spike glycoproteins assists virus infection (Peng et al, 2020). Inhibiting the interaction between the SARS-CoV-2 spike protein and the host cell receptor GRP78 would likely decrease the rate of viral infection (Ibrahim et al, 2020). Detecting specific genotype can help clinicians to predict collapsing glomerulopathy and the rates of kidney failure
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