COVID-19 induced renal injury differs from that in other viral-infections

Abstract

Background:Kidney injuries caused by several viral diseases have been reported worldwide among all age groups, races, and genders. Of particular importance is coronavirus disease 2019 (COVID-19), and its prevalence in communities infecting all patient populations with symptoms ranging from asymptomatic to severe, including complications and mortality.Methods:Data were acquired from PubMed, Scopus, Google Scholar, Centers for Disease Prevention and Control (CDC), and Lexi-Comp using the following search terms: “COVID-19 and renal pathology,” “COVID-19 induced kidney disease,” “Viral infection induced kidney disease,” and “Viral infection induced renal damage.” Titles and abstracts were manually analyzed as per the exclusion and inclusion criteria of relevant articles; relevance of articles included studies on the pathology of a specific viral infection and the impact of the virus on the adult renal system.Results:The mechanisms for renal disease due to COVID-19 include direct renal tubular injury, cytokine storm, inflammation, thrombosis vs. acute tubular necrosis, thrombotic events, and direct renal injury. Although some mechanisms behind renal dysfunction among the studied viral infections are similar, the prevalence rates of kidney injury or damage differ. This might be described by recommended prophylactic and therapeutic approaches that can alter the viral infection characteristics and possibly the impact a particular organ system.Conclusion:The patient population at risk was old in age and had a high body mass index. The mechanisms associated with renal dysfunction are similar, including direct renal injury through angiotensin converting enzyme 2 (ACE2) entry, inflammation, and thrombosis. The renal pathology of coronaviruses that differs from that of other prevalent viral infections is the activation of cytokine storm, which causes elevations of a greater number and different kinds of cytokines than other viral infections.

A scientific perspective of how and why Omicron is less severe than SARS-CoV-2

“…Skin rashes and discolored toes can also occur in COVID-19 infection, dependent on the patient’s age. [8] The pathology is not well understood. There are many ophthalmic complications, such as conjunctivitis, episcleritis, itchy eyes, and blurry vision, likely due to cytokine release syndrome or local invasion and inflammation.…”

“…Mutations in the RBD and N-terminal domain regions result in enhanced affinity of the spike protein binding to angiotensin-converting enzyme 2 (ACE2) and transmembrane serine protease 2 (TMPRSS2) receptors, which supplements viral attachment and entry into the host cells for infection. [8] A preprint reported 50 genetic mutations of Omicron, with 15 mutations occurring in the RBD of the spike protein, which binds to the ACE2 receptor for viral entry. [9] Experimental microscale thermophoresis data from this study further confirmed that the RBD mutations in Omicron are associated with a 5-fold higher binding affinity to ACE2 compared with the RBD of the original SARS-CoV-2 virus.…”

Acute kidney injury in patients with COVID-19 compared to those with influenza: a systematic review and meta-analysis

“…Direct cytopathic effects of a replicating virus, inflammation-induced cell injury from infiltrating inflammatory cells, acute tubule necrosis and podocyte damage contribute to protein leakage from the Bowman’s capsule and occurrence of collapsing glomerulopathy ( 43 ). COVID-19 infection can activate complement (C5b-9) deposition at the brush borders of apical tubules, leading to cell apoptosis, tubulointerstitial damage and impairment of renal function ( 44 , 45 ). Cytotoxic particles such as perforin, granulysin released by activated killer lymphocytes and leukocyte-derived proinflammatory cytokines such as interleukin-1, interleukin-6 and tumor necrosis factor-alpha, further lead to a cytokine storm.…”