ReviewThe journal of venomous animals and toxins including tropical diseases2021
Inflammation and kidney involvement in human viral diseases caused by SARS-CoV-2, HIV, HCV and HBV.
Review in The journal of venomous animals and toxins including tropical diseases, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Cardiorenal outcomes after herpes zoster reactivation in COVID-19 survivors from a global TriNetX study.Scientific reports · 2025Article
- Targeting hepatitis B virus-associated nephropathy: efficacy and challenges of current antiviral treatments.Clinical and experimental medicine · 2025Review
- Serum chemokine IL-8 acts as a biomarker for identifying COVID-19-associated persistent severe acute kidney injury.Renal failure · 2024Article
- Emerging fatal gout disease in Chinese goslings linked to acute kidney injury induced by novel goose astrovirus infection.Frontiers in cellular and infection microbiology · 2024Article
- Inflammasomes: a rising star on the horizon of COVID-19 pathophysiology.Frontiers in immunology · 2023Review
- Shared miRNA landscapes of COVID-19 and neurodegeneration confirm neuroinflammation as an important overlapping feature.Frontiers in molecular neuroscience · 2023Article
- A spotlight on HCV and SARS-CoV-2 co-infection and brain function.Pharmacology, biochemistry, and behavior · 2022Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammation is closely related to renal diseases. This is particularly true for renal diseases caused by infections as in viral diseases. In this review, we highlight the inflammatory mechanisms that underlie kidney dysfunction in SARS-CoV-2, human immunodeficiency (HIV), hepatitis C (HCV), and hepatitis B (HBV) infections. The pathophysiology of renal involvement in COVID-19 is complex, but kidney damage is frequent, and the prognosis is worse when it happens. Virus-like particles were demonstrated mostly in renal tubular epithelial cells and podocytes, which suggest that SARS-CoV-2 directly affects the kidneys. SARS-CoV-2 uses the angiotensin-converting enzyme 2 receptor, which is found in endothelial cells, to infect the human host cells. Critical patients with SARS-CoV-2-associated acute kidney injury (AKI) show an increase in inflammatory cytokines (IL-1β, IL-8, IFN-γ, TNF-α), known as cytokine storm that favors renal dysfunction by causing intrarenal inflammation, increased vascular permeability, volume depletion, thromboembolic events in microvasculature and persistent local inflammation. Besides AKI, SARS-CoV-2 can also cause glomerular disease, as other viral infections such as in HIV, HBV and HCV. HIV-infected patients present chronic inflammation that can lead to a number of renal diseases. Proinflammatory cytokines and TNF-induced apoptosis are some of the underlying mechanisms that may explain the virus-induced renal diseases that are here reviewed.
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