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A Large Animal Model for Acute Kidney Injury by Temporary Bilateral Renal Artery Occlusion
Published on: February 2, 2021
Acute Kidney Injury in COVID-19: a Brief Review
Vishwajeet Singh1, Mukul Kumar Singh1
1Department of Urology, King George's Medical University, Lucknow, UP 226003 India.
Insights
The COVID-19 virus enters cells via the ACE-2 receptor, damaging lungs and potentially kidneys. Early monitoring of kidney function is crucial to prevent acute kidney injury (AKI) and reduce mortality in COVID-19 patients.
Area of Science:
- Virology and Immunology
- Nephrology
Background:
- Coronavirus disease 2019 (COVID-19) poses a global health emergency due to high transmission, morbidity, and mortality.
- COVID-19 infection involves the angiotensin-converting enzyme 2 (ACE-2) receptor, leading to respiratory system damage and failure.
- Elevated pro-inflammatory cytokines, such as IL-6, IL-8, and TNF-alpha, are associated with COVID-19 pathogenesis.
Purpose of the Study:
- To review the association between COVID-19 and acute kidney injury (AKI).
- To highlight the importance of lung-kidney crosstalk in COVID-19 pathogenesis.
- To emphasize the need for critical monitoring of kidney function in COVID-19 patients.
Main Methods:
- Literature review of studies on COVID-19, ACE-2 receptors, and kidney injury.
- Analysis of molecular mechanisms involved in lung-kidney crosstalk.
- Examination of clinical data regarding COVID-19 patient outcomes and AKI.
Main Results:
- The ACE-2 receptor, crucial for viral entry, is also present in the kidneys, increasing AKI risk.
- Lung-kidney crosstalk, driven by inflammatory cytokines, contributes to kidney damage in COVID-19.
- A significant mortality rate in COVID-19 patients is linked to AKI.
Conclusions:
- Acute kidney injury (AKI) is a critical complication of COVID-19, associated with increased mortality.
- Monitoring kidney function and early clinical intervention are essential to mitigate kidney damage in COVID-19.
- Understanding the role of ACE-2 receptors and inflammatory pathways is vital for managing COVID-19 complications.
Abstract:
The contemporary evolution of the coronavirus disease 2019 (COVID-19) outbreak from the Wuhan, China, with a high rate of transmission will act the global medical emergency with immense morbidity and mortality rate across the world. The cell entry of COVID-19 via angiotensin-converting enzyme 2 receptor (ACE-2 receptor) will damage the respiratory system by the cytopathic effect induced by replication of the virus genome in the host and respond respiratory failure with an elevation of cytokine factor-like interleukin (IL) IL-6, IL-8, tumor necrosis factor-alpha (TNF-alpha), etc. However, the lung-kidney cross talk will evidence the activation of molecular mechanisms from pro-inflammatory cytokines and concerned with kidney damage, though the elevated rate of ACE-2 receptor in the kidney will enhance the possibility of mortality with consideration of acute kidney injury. This review provides relevant information which suggests the rate of mortality in COVID-19 patient associated with acute kidney injury (AKI) which lacks critical monitoring of kidney function with a clinical consideration of intervention to avoid kidney damage in the initial stage of the disease.
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