Pathophysiology of COVID-19-associated acute kidney injury

TY - JOUR

T1 - Pathophysiology of COVID-19-associated acute kidney injury

AU - Legrand, Matthieu

AU - Bell, Samira

AU - Forni, Lui

AU - Joannidis, Michael

AU - Koyner, Jay L.

AU - Liu, Kathleen

AU - Cantaluppi, Vincenzo

N1 - Publisher Copyright: © 2021, Springer Nature Limited.

PY - 2021/11

Y1 - 2021/11

N2 - 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.

AB - 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.

KW - Acute kidney injury

KW - Infectious diseases

KW - Kidney

KW - SARS-CoV-2

UR - https://www.scopus.com/pages/publications/85109866360

U2 - 10.1038/s41581-021-00452-0

DO - 10.1038/s41581-021-00452-0

M3 - Review article

C2 - 34226718

AN - SCOPUS:85109866360

SN - 1759-5061

VL - 17

SP - 751

EP - 764

JO - Nature Reviews Nephrology

JF - Nature Reviews Nephrology

ER -