Abstract
Kidney is one of the most predominantly organs affected by coronavirus disease 2019 (COVID-19) after the respiratory and immune systems. Among the renal parenchymal components, the tubulointerstitial compartment is presumed to be the prime target of injury in COVID-19. The main mechanism of renal tubular damage by COVID-19 is considered to be indirect, i.e., cytokine-mediated injury. A proportion of infected individuals mount a strong inflammatory response to the virus by an exaggerated immune response of the body, namely cytokine storm. Sudden and massive release of cytokines may lead to serious systemic hyper-inflammation and renal tubular injury and inflammation resulting in acute renal failure. In addition, a number of cases of glomerulopathies, particularly collapsing glomerulopathy (CG) have been reported, predominantly in people of African ancestry, as a rare form of kidney involvement by SARS-CoV-2 that may originate from the background genetic susceptibility in this population complicated by the second hit of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, either directly or indirectly. It is noteworthy that renal injury in COVID-19 could be severe in individuals of African origin due to the aforementioned genetic susceptibility, especially the presence of high-risk apolipoprotein L1 (APOL1) genotypes. Although the exact mechanism of kidney injury by SARS-CoV-2 is as yet unknown, multiple mechanisms are likely involved in renal damage caused by this virus. This review was aimed to summarize the salient points of pathogenesis of kidney injury, particularly glomerular injury in COVID-19 disease in the light of published data. A clear understanding of these is imperative for the proper management of these cases. For this review, a search was made of Google Scholar, Web of Science, Scopus, EBSCO and PubMed for finding English language articles related to COVID-19, kidney injury and glomerulopathy. From the information given in finally selected papers, the key aspects regarding glomerular involvement in COVID-19 were drawn out and are presented in this descriptive review.
Highlights
Coronavirus disease 2019 (COVID-19) is an emerging human infectious disease caused by a novel β-coronavirus, named severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)
It is noteworthy that renal injury in COVID-19 could be severe in individuals of African origin due to the aforementioned genetic susceptibility, especially the presence of high-risk apolipoprotein L1 (APOL1) genotypes
The ACE polymorphism and vulnerability to COVID-19 can clarify the serious forms of SARS-CoV-2 among African American population versus the Caucasian population
Summary
Coronavirus disease 2019 (COVID-19) is an emerging human infectious disease caused by a novel β-coronavirus, named severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). It was first detected in Wuhan, China, in December 2019, it soon spread throughout the world and since over 13 million people around the world have been affected by the pandemic [1]. The predominant organ involvement in individuals with SARS-CoV-2 is lung, which presents as a diffuse alveolar injury and pulmonary failure in severe cases [2]. ACE2 is abundantly expressed in renal tissue, in the proximal renal tubular cells. The D allele of ACE1 is linked to diminished expression of ACE2 [7]
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