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Global Translational Medicine COVID-19 and acute kidney injury

4. Discussion by corresponding clinical parameters in SARS patients. 19,20
In addition, circulating ACE2 levels have been reported to
COVID-19, the disease caused by the novel coronavirus, be higher in men than in women. 12
has affected 213 countries worldwide, infecting nearly
seven million people and resulting in nearly half a million In‐hospital mortality was higher among the AKI patients
deaths. The COVID-19 outbreak began in Wuhan, Hubei we analyzed. Multiple organ dysfunction, including in the
province, China, in December 2019 and rapidly spread liver, gastrointestinal tract, and kidneys, has been reported
21
globally. It is now well established that the novel coronavirus in patients with COVID-19. One possible explanation
is more dangerous than a common respiratory virus. is that some COVID-19 patients had a history of chronic
While it primarily targets the lungs, it can affect multiple kidney disease. In addition, some studies observed that the
organs throughout the body. Physicians have observed that median period between the onset of COVID-19 symptoms
22
it can cause blood clots and multiorgan failure. Notably, a and hospital admission was around a week. By this time,
subset of COVID-19 patients develops AKI despite normal patients may have developed a pro-inflammatory condition
creatinine levels, which can bypass standard screening with abnormalities in cellular populations, especially
21
criteria, often leading to fatal outcomes before detection. 17 immune cells. This delay in admission also increases the
risk of upper respiratory tract infections and pneumonia. 23,24
Our meta-analysis provides evidence that the incidence 2
of AKI in hospitalized COVID-19 patients is relatively low, Cheng et al. also noted that many COVID-19 patients
could not be admitted in the early stage of the disease due
at approximately 8%. However, the presence of AKI during to a lack of hospital beds. Earlier admission to the hospital
this viral infection signals a serious risk: in-hospital mortality could help physicians manage patients effectively and
among COVID-19 patients who developed AKI can reach up prevent the spread of nosocomial infection. 22
to 45%. Furthermore, our pooled calculation reveals that the
risk of death for COVID-19 patients with AKI is significantly There is evidence that severe COVID-19 patients have
elevated – about four times higher than for those without elevated levels of inflammatory cytokines such as IL-1RA,
AKI. Therefore, clinicians should pay special attention to the IL-7, IL-8, IL-9, and IL-10. 25,26 These cytokines may
treatment of COVID‐19 patients with severe AKI. contribute to the development of AKI in COVID-19 patients
by interacting with kidney cells and triggering endothelial
In this meta-analysis, we analyzed five studies, all of
which reported that older age and male sex are risk factors and tubular abnormalities. For instance, TNF-α has been
reported to bind to tubular cell receptors, triggering
for severe COVID-19. This finding is consistent with other 27
studies. For example, a case series conducted at Wuhan the death receptor pathway of apoptosis. In addition,
Union Hospital, Beijing, China, from January 29, 2020, studies have observed elevated IL-6 levels in seriously
to February 15, 2020, involving 43 COVID-19 patients, ill COVID-19 patients, with higher IL-6 levels noted in
deceased patients compared to survivors. The lethal role
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observed that older patients (≥65 years) were more of IL-6 has been demonstrated in different models. 29,30
likely to develop severe forms of COVID-19, and males Therefore, it is plausible that these cytokines play a role in
tended to develop more severe cases than females. In a the development of AKI in COVID-19 patients.
comparable public dataset of COVID-19, it was found that
the percentage of older adults (≥65 years) was much higher We also found that COVID-19 patients generally
among deceased patients than among survivors (83.8% exhibited kidney disorders, characterized by elevated
in 37 deceased patients vs. 13.2% in 1019 survivors). In levels of serum creatinine, and blood urea nitrogen, along
18
addition, the number of men among the deceased was about with proteinuria and hematuria. The occurrence of kidney
two and a half times higher than that of women. Although disorders in COVID-19 patients might be explained by
men and women have similar vulnerability to infection, several factors. SARS-CoV-2 uses ACE2 as a cell entry
males are more prone to death. Therefore, gender plays a receptor. This receptor is abundantly expressed in the
28
vital role in COVID-19 case fatality. This gender disparity, small intestine, testis, kidneys, heart, thyroid, and adipose
along with higher incidence rates of severe disease in tissue, with higher expression levels in the kidney than
31
men, may correlate with the general demographic trend in the lung. Therefore, it is likely that SARS-CoV-2 can
8
of shorter life expectancy in men compared to women, directly infect kidney epithelial cells, in addition to lung
both in China and globally. Other studies from the Beijing epithelial cells. This hypothesis is supported by recent
32
Municipal Medical Taskforce have indicated that SARS- histology reports of renal tissues from autopsies, which
CoV-2 infects cells through the angiotensin-converting found acute renal tubular damage in six COVID-19 cases.
33
enzyme 2 (ACE2) receptor. It was previously reported that Kidney disorders, along with other organ involvement, can
high protein expression of the ACE2 receptor in specific exacerbate the inflammatory process, leading to injury and
organs correlates with specific organ failures, as indicated death of renal tubular epithelial cells. 34

Volume 3 Issue 3 (2024) 9 doi: 10.36922/gtm.2798