Nephrologic Disorders and COVID-19: Difference between revisions

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====Clinical Features of AKI by SARS-CoV-2====
====Clinical Features of AKI by SARS-CoV-2====
====Treatment====
====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<ref name="pmid32416769">{{cite journal| author=Ronco C, Reis T, Husain-Syed F| title=Management of acute kidney injury in patients with COVID-19. | journal=Lancet Respir Med | year= 2020 | volume=  | issue=  | pages=  | pmid=32416769 | doi=10.1016/S2213-2600(20)30229-0 | pmc=7255232 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=32416769  }} </ref>:
**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

Revision as of 02:54, 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.

Clinical Features of AKI by SARS-CoV-2

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[2]:
    • 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
  1. ↑ 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.
  2. ↑ Ronco C, Reis T, Husain-Syed F (2020). "Management of acute kidney injury in patients with COVID-19". Lancet Respir Med. doi:10.1016/S2213-2600(20)30229-0. PMC 7255232 Check |pmc= value (help). PMID 32416769 Check |pmid= value (help).
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