Renin-angiotensin system inhibitors in COVID-19

Thomas, George

doi:10.3949/ccjm.87a.ccc009

Cited by 8 publications

(8 citation statements)

References 17 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…There was some controversy regarding the use of ACE1inhibitors (ACE-I) and angiotensin II-receptor blockers (ARBs) in patients with COVID-19 since both are known to increase ACE2 level that is the receptor for SARS-CoV-2 [139]. However, since the primary pathology is due to the loss of ACE2, it stands to reason that ACE-I and ARBs can be helpful [140].…”

Section: Raas Inhibitorsmentioning

confidence: 99%

Thrombosis in Coronavirus disease 2019 (COVID-19) through the prism of Virchow’s triad

2020

View full text Add to dashboard Cite

The pathogenesis of Coronavirus disease 2019 (COVID-19) is gradually being comprehended. A high number of thrombotic episodes are reported, along with the mortality benefits of heparin. COVID-19 can be viewed as a prothrombotic disease. We overviewed the available evidence to explore this possibility. We identified various histopathology reports and clinical case series reporting thromboses in COVID-19. Also, multiple coagulation markers support this. COVID-19 can be regarded as a risk factor for thrombosis. Applying the principles of Virchow's triad, we described abnormalities in the vascular endothelium, altered blood flow, and platelet function abnormalities that lead to venous and arterial thromboses in COVID-19. Endothelial dysfunction, activation of the renin-angiotensin-aldosterone system (RAAS) with the release of procoagulant plasminogen activator inhibitor (PAI-1), and hyperimmune response with activated platelets seem to be significant contributors to thrombogenesis in COVID-19. Stratifying risk of COVID-19 thromboses should be based on age, presence of comorbidities, D-dimer, CT scoring, and various blood cell ratios. Isolated heparin therapy may not be sufficient to combat thrombosis in this disease. There is an urgent need to explore newer avenues like activated protein C, PAI-1 antagonists, and tissue plasminogen activators (tPA). These should be augmented with therapies targeting RAAS, antiplatelet drugs, repurposed antiinflammatory, and antirheumatic drugs.

show abstract

Section: Raas Inhibitorsmentioning

confidence: 99%

Thrombosis in Coronavirus disease 2019 (COVID-19) through the prism of Virchow’s triad

2020

View full text Add to dashboard Cite

show abstract

“…Because SARS-CoV-2 is found in the urine, kidney damage pattern caused by the virus is limited to areas with ACE2 receptor, and the time course in which the virus appears in the urine coincides with the onset of AKI, so it was suggested that the virus directly affects the kidneys [35] , [36] , [37] . The virus is claimed to enter the kidney cell by binding to membrane-bound ACE2 receptors in the glomerular podocyte cells and the apical membrane of proximal tubule cells, and in addition to damaging the kidney epithelial cells, it disarranges the balance of renin-angiotensin system [38] . The angiotensinogen is primarily converted to angiotensin-I by renin and then to angiotensin-II under the influence of angiotensin-converting enzyme (ACE).…”

Section: Epidemiology and Pathophysiology Of Covid-19 Induced Acute Kidney Injurymentioning

confidence: 99%

“…If SARS-CoV-2 occupies ACE2, angiotensin-II levels increase, leading to vasoconstriction, glomerular dysfunction, inflammation, and fibrosis [38] , [39] .Recently Wang et al and Chiu et al found that SARS-CoV-2 also invades host cells via CD 147-spike protein pathway and this glycoprotein is highly expressed in proximal tubule [40] , [41] . Moreover, SARS-CoV-2 causes kidney damage by activating inflammatory pathways and cytokine storm, activating coagulation pathways, damage to renal vascular endothelium, sepsis, hemodynamic instability as well as hypoxemia [38] , [42] , [43] . Viral infection of endothelium via immune cell recruitment causes defective endothelial function and reduces the production of vasodilators, including the nitric oxide.…”

Section: Epidemiology and Pathophysiology Of Covid-19 Induced Acute Kidney Injurymentioning

confidence: 99%

Kidney injury in COVID-19 patients, drug development and their renal complications: Review study

Yarijani

Najafi

2021

Biomedicine & Pharmacotherapy

View full text Add to dashboard Cite

Since December 2019, the world was encountered a new disease called coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Although SARS-CoV-2 initially causes lung damage, it also affects many other organs, including the kidneys, and on average, 5 to 23% of people with COVID-19 develop the symptoms of acute kidney injury (AKI), including elevated blood creatinine and urea, hematuria, proteinuria, and histopathological damages. The exact mechanism is unknown, but the researchers believe that SARS-CoV-2 directly and indirectly affects the kidneys. The direct pathway is by binding the virus to ACE2 receptor in the kidney, damage to cells, the renin-angiotensin system disturbances, activating coagulation pathways, and damaging the renal vascular endothelium. The initial evidence from studying the kidney tissue in postmortem patients is more in favor of the direct pathway. The indirect pathway is created by increased cytokines and cytokine storm, sepsis, circulatory disturbances, hypoxemia, as well as using the nephrotoxic drugs. Using renal tissue biopsy and autopsy in the patients with COVID-19, recent studies found evidence for a predominant indirect pathway in AKI induction by SARS-CoV-2. Besides, some studies showed that the degree of acute tubular injury (ATI) in autopsies from COVID-19 victims is milder compared to AKI degree. We review the mechanism of AKI induction and the renal side effects of the most common drugs used to treat COVID-19 after the overview of the latest findings on SARS-CoV-2 pathogenicity.

show abstract

“…These will need individual management since some medications, specifically ACE inhibitors, are associated with a poor response to COVID-19 infection. 18–21 It is suggested that Vitamin D supplementation may be a prophylactic measure, particularly for BAME personnel, but this remains unproven. We would also suggest that even non-diabetic staff with the Metabolic Syndrome be offered treatment with Metformin.…”

Section: Uk Experiencementioning

confidence: 99%

Occupational risk prevention, education and support in black, Asian and ethnic minority health worker in the COVID-19 pandemic

Morris

Elneil

Morris

et al. 2020

Journal of Patient Safety and Risk Management

View full text Add to dashboard Cite

The onset of the COVID-19 in the UK has resulted in an inordinate amount of deaths affecting Black, Asian and Ethnic Minority (BAME) healthcare workers. The occupational risk to this group is thought to be a contributory factor, but other factors include race, genetics, medical co-morbidities, socio-economic status, and access to personal protection equipment. Why COVID-19 appears to be more deadly in BAME members remains unknown, but the UK government is investigating this now. It does appear that certain factors may worsen the disease process in BAME members, but which ones are pertinent to prevention remain to be determined, until a vaccine is available. Thus, the onus should rest on risk prevention, education, and support for all. Some of the safety strategies that may be instituted to help guide those in the workplace include education, treating potential therapeutic targets and ensuring protection in the working environment. The consideration of a compensation scheme, for families of healthcare workers that have suffered because of COVID-19, would go some way to support the recovery process.

show abstract

Renin-angiotensin system inhibitors in COVID-19

Cited by 8 publications

References 17 publications

Thrombosis in Coronavirus disease 2019 (COVID-19) through the prism of Virchow’s triad

Thrombosis in Coronavirus disease 2019 (COVID-19) through the prism of Virchow’s triad

Kidney injury in COVID-19 patients, drug development and their renal complications: Review study

Occupational risk prevention, education and support in black, Asian and ethnic minority health worker in the COVID-19 pandemic

Contact Info

Product

Resources

About