Nephrologic Disorders and COVID-19

To go to the COVID-19 project topics list, click here.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Sogand Goudarzi, MD [2] Nasrin Nikravangolsefid, MD-MPH [3]

Complications

AKI

Pathophysiology

• Angiotensin-converting enzyme 2 (ACE2), which is a primary receptor for SARS-CoV-2 entry into cells, mostly presents in renal tubular epithelial cells as well as lungs and heart.
• Despite kidney injury following COVID-19 infection is less frequent than severe lung injury, ACE2: ACE ratio is higher in the kidneys compared to the respiratory system. (1:1 in the kidneys VS 1:20 in the respiratory system)
• After SARS-CoV-2 enters through the nasal cavity, it may travel to the kidneys and enters the bloodstream leading to severe inflammatory response activation and cytokine storm.
• It is thought that AKI following COVID-19 is the result of
  • Sepsis
  • Hypovolemia and Hypotension
  • Hypoxemia
  • Blood clots formation, leading to impaired blood flow in the renal arterioles.
• AKI often occurs at later stages in critically ill patients with COVID-19 following multiple organ failure.

Treatment

• Management of AKI following COVID-19 includes treatment of infection, identifying electrolyte disorders, and intravenous fluid administration.
• Treatment of AKI following COVID-19 includes:
  • Correction of hypovolemia and hypotension by the administration of adequate intravenous fluid
  • Correction of electrolyte disturbances
  • Renal Replacement Therapy
    • If AKI is unresponsive to conservative therapy
    • In volume overload conditions
    • Modality of choice in unstable hemodynamic status
  • Anticoagulants in hypercoagulable conditions
  • Sequential extracorporeal therapy