Renal Injury by SARS-CoV-2 Infection: A Systematic Review

Abstract

<b><i>Background:</i></b> SARS-CoV-2 infection can cause renal involvement, and severe renal dysfunction is more common among patients with chronic comorbid conditions, especially patients with chronic kidney disease. Angiotensin-converting enzyme 2 (ACE2) has been proven to be the major receptor of SARS-CoV-2 in kidneys, suggesting that ACE2-related changes may be involved in renal injury during the infection. In this review, we systematically reviewed the literature to summarize findings on the mechanism of renal injury caused by SARS-COV-2 infection, in order to provide a theoretical basis for renal protection therapy. <b><i>Summary:</i></b> For patients with SARS-CoV-2 infection, renal injury mainly manifests as increased serum creatinine, variable degrees of proteinuria and hematuria, and radiographic abnormalities of the kidneys. In this review, we summarize the pathogenesis of renal injury deriving from SARS-CoV-2 infection by focusing on its etiology, pathology, and clinical manifestations. The virus causes kidney injury by either direct infection or systemic effects, including host immune clearance and immune tolerance disorders, endothelium-mediated vasculitis, thrombus formation, glucose and lipid metabolism disorder, and hypoxia. <b><i>Key Messages:</i></b> Renal injury by SARS-CoV-2 is the result of multiple factors. Via highly expressed ACE2 in renal tissue, SARS-CoV-2 infection fundamentally initiates a mechanism of renal injury. Systemic effects such as host immune clearance and immune tolerance disorders, endothelial cell injury, thrombus formation, glucose and lipid metabolism disorder, and hypoxia aggravate this renal injury.

Emerging Role of Neuropilin-1 and Angiotensin-Converting Enzyme-2 in Renal Carcinoma-Associated COVID-19 Pathogenesis

“…Many reports showed that SARS-CoV-2 might cause direct kidney injury due to the high expression of ACE2 in the renal tissue, and multiple factors such as endothelial cell injury, host immune clearance, and immune tolerance disorders, and lipid metabolic disorders, etc. promote kidney injury [ 7 , 23 , 24 ]. Previous reports also suggested that the newly identified SARS-CoV-2 host factor NRP1 mRNA and protein expression in the kidney also control the integrity of the glomerular basement membrane [ 25 , 26 ].…”

Urinary angiotensin converting enzyme 2 and disease activity in pediatric IgA nephropathy

“…The SARS-CoV-2 spike protein binds to membrane-bound ACE2 on the surface of respiratory epithelial cells to gain cell entry (17,18). SARS-CoV-2 infection can cause renal involvement, and severe renal dysfunction is more common among patients with chronic kidney disease (19). SARS-CoV-2 infection fundamentally initiates a mechanism of renal injury through highly expressed ACE2 in renal tissue, suggesting that ACE2 signaling pathway plays a key role in the development of the disease (19).…”

“…SARS-CoV-2 infection can cause renal involvement, and severe renal dysfunction is more common among patients with chronic kidney disease (19). SARS-CoV-2 infection fundamentally initiates a mechanism of renal injury through highly expressed ACE2 in renal tissue, suggesting that ACE2 signaling pathway plays a key role in the development of the disease (19). Furthermore, systemic effects such as host immune clearance and immune tolerance disorders, endothelial cell injury, thrombus formation, glucose and lipid metabolism disorder, and hypoxia aggravate this renal injury (19).…”

Revealed pathophysiological mechanisms of crosslinking interaction of affected vital organs in COVID-19

“…Through highly expressed ACE2 in renal tissue, SARS-CoV-2 infection fundamentally initiates a mechanism of renal injury. Systemic effects such as host immune clearance and immune tolerance disorders, endothelial cell injury, thrombus formation, glucose and lipid metabolism disorder, and hypoxia aggravate this renal injury (Wang et al 2020b). Due to severe but huge number of COVID-19 patients and the associated complications make it hard to manage patients on dialysis and during kidney transplantation (Alberici et al 2020).…”