Pathophysiology of COVID-19-associated acute kidney injury

Matthieu Legrand (Lead / Corresponding author), Samira Bell, Lui Forni, Michael Joannidis, Jay L. Koyner, Kathleen Liu, Vincenzo Cantaluppi

Research output: Contribution to journalReview articlepeer-review

1 Citation (Scopus)

Abstract

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.

Original languageEnglish
Number of pages14
JournalNature Reviews Nephrology
Early online date5 Jul 2021
DOIs
Publication statusE-pub ahead of print - 5 Jul 2021

Keywords

  • Acute kidney injury
  • Infectious diseases
  • Kidney
  • SARS-CoV-2

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