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Pathophysiology of COVID-19-associated acute kidney injury
by
Legrand Matthieu
, Joannidis, Michael
, Koyner, Jay L
, Liu, Kathleen
, ni Lui
, Bell, Samira
, Cantaluppi Vincenzo
in
Coronaviruses
/ COVID-19
/ Kidneys
/ Pathophysiology
/ Respiratory failure
/ Severe acute respiratory syndrome coronavirus 2
2021
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Pathophysiology of COVID-19-associated acute kidney injury
by
Legrand Matthieu
, Joannidis, Michael
, Koyner, Jay L
, Liu, Kathleen
, ni Lui
, Bell, Samira
, Cantaluppi Vincenzo
in
Coronaviruses
/ COVID-19
/ Kidneys
/ Pathophysiology
/ Respiratory failure
/ Severe acute respiratory syndrome coronavirus 2
2021
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Do you wish to request the book?
Pathophysiology of COVID-19-associated acute kidney injury
by
Legrand Matthieu
, Joannidis, Michael
, Koyner, Jay L
, Liu, Kathleen
, ni Lui
, Bell, Samira
, Cantaluppi Vincenzo
in
Coronaviruses
/ COVID-19
/ Kidneys
/ Pathophysiology
/ Respiratory failure
/ Severe acute respiratory syndrome coronavirus 2
2021
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Pathophysiology of COVID-19-associated acute kidney injury
Journal Article
Pathophysiology of COVID-19-associated acute kidney injury
2021
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Overview
Although respiratory failure and hypoxaemia are the main manifestations of COVID-19, kidney involvement is also common. Available evidence supports a number of potential pathophysiological pathways through which acute kidney injury (AKI) can develop in the context of SARS-CoV-2 infection. Histopathological findings have highlighted both similarities and differences between AKI in patients with COVID-19 and in those with AKI in non-COVID-related sepsis. Acute tubular injury is common, although it is often mild, despite markedly reduced kidney function. Systemic haemodynamic instability very likely contributes to tubular injury. Despite descriptions of COVID-19 as a cytokine storm syndrome, levels of circulating cytokines are often lower in patients with COVID-19 than in patients with acute respiratory distress syndrome with causes other than COVID-19. Tissue inflammation and local immune cell infiltration have been repeatedly observed and might have a critical role in kidney injury, as might endothelial injury and microvascular thrombi. Findings of high viral load in patients who have died with AKI suggest a contribution of viral invasion in the kidneys, although the issue of renal tropism remains controversial. An impaired type I interferon response has also been reported in patients with severe COVID-19. In light of these observations, the potential pathophysiological mechanisms of COVID-19-associated AKI may provide insights into therapeutic strategies.Acute kidney injury (AKI) is a common complication of COVID-19. This Review describes current understanding of the pathophysiology of COVID-19-associated AKI, examining potential mechanisms by which SARS-CoV-2 infection might induce direct and indirect effects on the kidney and non-specific factors, including haemodynamic changes and/or organ crosstalk, that may adversely influence kidney function.
Publisher
Nature Publishing Group
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