COVID-19 is primarily considered a respiratory illness, but the kidney may be one of the targets of SARS-CoV-2 infection since the virus enters cells through the angiotensin-converting enzyme 2 receptors, which is found in abundance in the kidney. This article discusses the pathogenesis of acute kidney injury (AKI) in COVID-19, its optimal management, and the impact of COVID-19 on patients with chronic kidney disease, patients with end-stage kidney disease on dialysis, and kidney transplant recipients.


Key points

  • AKI is common in COVID-19 and is associated with poor outcomes.
  • SARS-CoV-2 can damage the kidney through several mechanisms, including acute lung injury, sepsis, hemodynamic alterations, cytotoxic effects, cytokine release syndrome, rhabdomyolysis, coagulopathy, microangiopathy, and collapsing glomerulopathy.
  • Despite initial speculation, renin-angiotensin-aldosterone system inhibitors need not be discontinued in patients with COVID-19.
  • Treatment of AKI includes general management, pharmacologic management of COVID-19, hemodynamic and volume optimization, and extracorporeal therapies.
  • Pharmacotherapy for COVID-19 can be divided into antibacterial, antiviral, immunomodulatory, and anti-inflammatory drugs.