Nephrologic Disorders and COVID-19: Difference between revisions
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===AKI=== | ===AKI=== | ||
====Pathophysiology==== | ====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.<ref name="MalhaMueller2020">{{cite journal|last1=Malha|first1=Line|last2=Mueller|first2=Franco B.|last3=Pecker|first3=Mark S.|last4=Mann|first4=Samuel J.|last5=August|first5=Phyllis|last6=Feig|first6=Peter U.|title=COVID-19 and the Renin-Angiotensin System|journal=Kidney International Reports|volume=5|issue=5|year=2020|pages=563–565|issn=24680249|doi=10.1016/j.ekir.2020.03.024}}</ref> | |||
*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)<ref name="MalhaMueller2020">{{cite journal|last1=Malha|first1=Line|last2=Mueller|first2=Franco B.|last3=Pecker|first3=Mark S.|last4=Mann|first4=Samuel J.|last5=August|first5=Phyllis|last6=Feig|first6=Peter U.|title=COVID-19 and the Renin-Angiotensin System|journal=Kidney International Reports|volume=5|issue=5|year=2020|pages=563–565|issn=24680249|doi=10.1016/j.ekir.2020.03.024}}</ref> | |||
* 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<ref name="MalhaMueller2020">{{cite journal|last1=Malha|first1=Line|last2=Mueller|first2=Franco B.|last3=Pecker|first3=Mark S.|last4=Mann|first4=Samuel J.|last5=August|first5=Phyllis|last6=Feig|first6=Peter U.|title=COVID-19 and the Renin-Angiotensin System|journal=Kidney International Reports|volume=5|issue=5|year=2020|pages=563–565|issn=24680249|doi=10.1016/j.ekir.2020.03.024}}</ref> | |||
**[[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. | |||
[[File:AKI physiopathology COVID.PNG|600px|center]] | |||
====Clinical Features of AKI by SARS-CoV-2==== | ====Clinical Features of AKI by SARS-CoV-2==== | ||
====Treatment==== | ====Treatment==== | ||
Revision as of 02:51, 22 June 2020
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]
Overview
Nephrologic_Disorders of COVID-19
Nephrologic_Disorders risk factors of COVID-19
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.[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.
