Nephrologic Disorders and COVID-19

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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]

Overview

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.^[1]
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)^[1]
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^[1]
- 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.

↑ ^1.0 ^1.1 ^1.2 Malha, Line; Mueller, Franco B.; Pecker, Mark S.; Mann, Samuel J.; August, Phyllis; Feig, Peter U. (2020). "COVID-19 and the Renin-Angiotensin System". Kidney International Reports. 5 (5): 563–565. doi:10.1016/j.ekir.2020.03.024. ISSN 2468-0249.