Page 61 - GTM-3-3

Global Translational Medicine COVID-19 and acute kidney injury

Table 6. Results of quality assessment for risk of selection bias as per Newcastle–Ottawa scale
Study Age Gender Sampling method Location Author, year Total scores Risk of selection bias
Lim et al. 5 1 1 1 1 1 5 Low risk
Shao et al. 6 1 1 1 1 1 5 Low risk
Cheng et al. 2 1 1 1 1 1 5 Low risk
Wang et al. 7 1 1 1 1 1 5 Low risk

Figure 4. Mechanism of acute kidney injury in COVID-19 infection.
Figure created with MS Word

3.5.2. Endothelial damage
The immune response to the virus can result in endothelial
dysfunction, compromising the integrity of the blood–
Figure 3. Funnel plot for the selection of studies for qualitative analysis. kidney barrier. 14
Figure created with MedCalc
3.5.3. Immune dysregulation
3.4.9. Proteinuria and hematuria A cytokine storm, characterized by the overproduction
Proteinuria (the presence of protein in the urine) and of pro-inflammatory cytokines, can disrupt the balance
hematuria (the presence of blood in the urine) are common of the immune system, leading to systemic inflammation
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indicators of kidney injury. Studies have reported that and kidney injury. A literature review specifically
43.9% of hospitalized COVID-19 patients had proteinuria, examined the circulating levels of immune mediators in
and 26.7% exhibited hematuria upon admission. Moreover, COVID-19 patients, both those with and without AKI.
the prevalence of elevated blood urea nitrogen and serum The study found significant alterations in the levels of pro-
creatinine was reported at 13.1% and 14.4%, respectively. 12 inflammatory cytokines, chemokines, and growth factors
among AKI patients compared to those without AKI. These
3.5. Discussion on immune parameters and changes include higher levels of C–C motif chemokine
pathophysiology ligand (CCL)-2, CCL-3, CCL-4, C-X-C chemokine ligand
The discussion on immune parameters and pathophysiology (CXCL)-8, CXCL-10, interferon (IFN)-γ, IL-2, IL-6, TNF-α,
in COVID-19 patients with AKI highlights the complex IL-1Ra, IL-10, and vascular endothelial growth factor among
interplay between viral infection, immune response, AKI patients compared to those without AKI. These immune
and kidney function. The studies by Shao et al., Cheng mediators were also associated with each other and with the
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et al., Wang et al., Li et al., and others collectively suggest SARS-CoV-2 viral load in AKI patients, suggesting that the
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that immune dysregulation, particularly the presence of a loss of immunological homeostasis significantly contributes
cytokine storm, plays a significant role in the development to the development of kidney injury in COVID-19.
of AKI in COVID-19 patients. 2,6-8 The pathophysiology Furthermore, the study found that early alterations
of AKI in COVID-19 involves multiple mechanisms in CCL-2, CXCL-8, CXCL-10, IFN-γ, IL-6, IL-1Ra, and
(Figure 4): IL-10 have good predictive value for AKI development.
These findings underscore the importance of monitoring
3.5.1. Direct viral infection of renal cells immune parameters in COVID-19 patients, as they could
SARS-CoV-2 can directly infect renal cells, leading to potentially serve as predictive biomarkers for AKI and
cellular damage and impairment of kidney function. 13 mortality.

Volume 3 Issue 3 (2024) 8 doi: 10.36922/gtm.2798