Cardiorenal Disease in COVID-19 Patients

Sifaat, Muhtasham; Patel, Pinak; Sheikh, Razan; Ghaffar, Dawood; Vaishnav, Hitesh; Nahar, Ludmila; Rupani, Sonia; Quadri, Syed

doi:https://doi.org/10.1155/2022/4640788

Journal of the Renin-Angiotensin-Aldosterone System

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Abstract Introduction Conclusion Conflicts of Interest Authors’ Contributions Acknowledgments References Copyright Related Articles

Review Article | Open Access

Volume 2022 | Article ID 4640788 | https://doi.org/10.1155/2022/4640788

Cardiorenal Disease in COVID-19 Patients

Muhtasham Sifaat,¹Pinak Patel,¹Razan Sheikh,¹Dawood Ghaffar,¹Hitesh Vaishnav,¹Ludmila Nahar,²Sonia Rupani,³and Syed Quadri¹

Academic Editor: Vijaya Anand

Received20 Jan 2022

Revised28 Feb 2022

Accepted09 Mar 2022

Published18 Mar 2022

Abstract

Coronavirus disease 2019 (COVID-19) is an illness caused by a novel coronavirus called severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Mutations in the genetic coding and the variations in the spike proteins are critical for the virus’s mechanism of facilitating fusion with the human host, making the disease more severe. Recent research indicates that comorbidities including diabetes, hypertension, renal disease, heart failure, and atherosclerosis play a significant role in the severity and high mortality rates of (COVID-19), suggesting that perhaps the metabolic syndrome and its components are associated with COVID-19 morbidity. Primarily, angiotensin-converting enzyme 2 (ACE2) receptor is identified as the entrance receptor of SARS-CoV-2. Increased ACE2 expression, endothelial dysfunction plays a vital role in the progression and severity of complications developed due to COVID-19. In this review, we will discuss the association and management of cardiorenal disease and COVID-19.

1. Introduction

The novel coronavirus disease 2019 (COVID-19) is defined as an illness caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which has had a terrible effect on the world’s demography, resulting in the deaths of over 5.89 million people globally [1]. After the first case of this primarily respiratory viral illness was reported in late December 2019 in Wuhan, Hubei Province, China, SARS-CoV-2 quickly spread around the world, prompting the World Health Organization (WHO) to proclaim it a pandemic [2]. Despite significant progress in clinical research leading to a better understanding of SARS-CoV-2 and the management of COVID-19, limiting the virus and its variants’ continued spread has become an issue of increasing concern, as SARS-CoV-2 continues to wreak havoc around the world, with many countries experiencing a second or third wave of outbreaks especially attributed to the emergence of mutant viral strains.

While adapting to their new human hosts, SARS-CoV-2 is susceptible to genetic evolution with the formation of mutations over time, resulting in mutant variations with different characteristics than their ancestral strains. Novel Pfizer-BioNTech COVID-19 vaccine was recently approved by the Food and Drug Administration (FDA) [3]. Other vaccines and treatment have become available under emergency use authorization [4] to mitigate the spread and burden of COVID-19. However, their effectiveness and long-term outcomes are still to be determined. The emergence of newer SARS-CoV-2 variants could also threaten to undermine the significant progress made so far in limiting the spread of this viral infection [5].

The binding of spike protein to the ACE2 receptor leads to activation and progression of the infection [6]. The spike proteins cleave at the S1/S2 site after binding to ACE2, and the following cleavage of the S2 site enables the spike protein to fuse to the host membrane via irreversible conformational changes [7]. ACE2 is mainly expressed in the heart, lungs, intestinal epithelium, vascular endothelium, and kidneys, indicating its pivotal role in multiorgan dysfunction seen with SARS-CoV-2 infection [8, 9]. According to a recent study, COVID-19 is increasingly being linked to a higher risk of morbidity and mortality from cardiovascular disease (CVD) [10]. In this review, we will discuss the correlation between cardiorenal disease and COVID-19.

2. Methodology

The authors searched PubMed and Google Scholar for articles using the keywords “COVID-19”, “SARS-CoV-2”, “renin angiotensin aldosterone system”, “heart”, “cardiac”, “cardiovascular”, “heart failure”, “hypertension”, “atherosclerosis”, “kidney”, “renal dysfunction”, and “angiotion-converting enzyme inhibitors”. Case reports, systematic reviews and meta-analyses, clinical guidelines, and narrative reviews on COVID-19 and cardiovascular and renal effects and consequences were included. The research was limited to studies that were written in English.

3. COVID-19 in Cardiovascular Patients

Cardiovascular disease is the most prevalent comorbidity associated with COVID-19 [11]. In patients with CVD, COVID-19 can infect cardiac cells and cause significant heart damage through multiple mechanisms including an increase in renin-angiotensin aldosterone [12] system (RAAS) and proinflammatory mechanisms [13] leading to endothelial dysfunction, having a severe impact on their health [14, 15]. RAAS plays a vital role in blood pressure regulation and fluid balance. A hyperactive RAAS significantly increases angiotensin II which increases blood pressure and promotes sodium retention, vasoconstriction, oxidative stress resulting in ROS-mediated second messenger signaling, endothelial dysfunction, and organ damage [16, 17]. RAAS is also mediated by angiotensins 1-7 which counteracts the effects of angiotensin II [12, 18]. Angiotensin-converting enzyme 2 (ACE2) degrades angiotensin I (ang I) to inactive angiotensins 1-9 and angiotensin II (ang II) to angiotensins 1-7. Ang 1-7 exerts antioxidant, antifibrotic, vasodilators, and anti-inflammatory through Mas receptor [19] and counterbalances ACE-/ang II-mediated effects. ACE2 has been shown to mediate the viral entry of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) responsible for COVID-19 [6, 20]. This potentially leads to the reduction of ACE2, and the effects of ang II are augmented in the absence of RAAS-counterregulating mechanisms.

3.1. Hypertension

Data from China’s National Health Commission suggests that 35% of COVID-19 patients also had hypertension [21]. According to a study, comparing 126 COVID-19 patients with a preexisting hypertension to 125 age and gender-matched COVID-19 patients without hypertension concluded that hypertensive patients had 21.3% more severe SARS-CoV-2 infection and a higher mortality rate (10.3% vs 6.4%) [13]. A group of 191 COVID-19 patients from Wuhan, China, were studied, and hypertension was present in 48% of nonsurvivors [22]. In a group of 138 hospitalized patients, hypertension was present in 58% of patients requiring ICU admission [21] establishing that hypertension is a major risk factor with worse clinical outcomes. The exact mechanism underlying these interactions is unknown. However, in patients with SARS-CoV-2 infection, hypertension could potentially exacerbate the inflammatory profile indicating that hypertension raises the chance of a more severe illness as these patients have greater levels of inflammatory biomarkers including tumor necrosis-α (TNF-α) and interleukin-6 (IL-6) contributing to endothelial dysfunction and oxidative stress confirming a possible pathophysiological link between hypertension and COVID-19 [12, 23].

3.2. Heart Failure

In COVID-19 patients, heart failure is another major cause of mortality. The mechanism of COVID-19’s cardiac involvement is being investigated. Different myocardial mechanisms contribute to heart failure in COVID-19 patients, including direct myocardial involvement mediated by viral action [24]. Involvement of ACE2 was reported in a mouse model, SARS-CoV-2 infection resulted in an ACE2-dependent myocardial infection [25]. Another mechanism could be a potential cytokine storm, mediated by an unbalanced response across T helper cells [22], oxygen supply-demand imbalance, and hypoxia-induced increased intracellular calcium leading to cardiac myocyte death [21]. Proinflammatory biomarkers (D-dimer, ferritin, interleukin-6, and lactate dehydrogenase) and respiratory distress have been reported to exacerbate preexisting left ventricle (LV) failure or contribute to the development of new-onset cardiomyopathy [26]. Myocarditis, stress cardiomyopathy, or myocardial ischemia can all cause new-onset LV dysfunction. In a research by Zhou et al., nonsurvivors from COVID-19 had a higher rate of heart failure than survivors [22, 27]. Right heart failure is most likely caused by increased pulmonary artery pressure due to pulmonary dysfunctions. Exacerbation of heart failure with preserved ejection fraction can occur in the early stages of the disease due to vigorous fluid resuscitation attempts, and acute systolic heart failure leading to cardiogenic shock can occur in the advanced stages of the disease as cytokine levels rise [26, 27]. According to Guo et al., an increase in serum troponin in patients with or without previous cardiovascular disease was linked to an increase in plasmatic NT-proBNP levels, which increased mortality and was described as a poor prognostic marker [28]. As a result, heart disease is a significant risk factor for COVID-19 individuals.

3.3. Atherosclerosis

Inflammation has become a significant concern in COVID-19 patients encouraging the progression of atherosclerosis, leading to cardiovascular problems [29]. The primary issues associated with immunopathology in individuals with COVID-19 are dysregulation impacting T lymphocytes and an uncontrolled inflammatory process [30] supported by the fact that the blood samples from COVID-19 patients have reduced T lymphocyte, helper, and regulatory lines [31] resulting in uncontrolled inflammation. Another possible mechanism responsible for the inflammation in COVID-19 patients is cytokine storm [32, 33]. Recently, Huang et al. reported that interleukins (IL-1β, IL-7, IL-8, IL-9, and IL-10), fibroblast growth factor (FGF), tumor necrosis factor-α (TNF-α), granulocyte colony-stimulating factor (G-CSF), interferon (IFN), monocyte chemoattractant protein (MCP1), and macrophage inflammatory protein 1-α (MIP1-α) were significantly upregulated in the COVID-19 patients [34] An increase in von Willebrand factor antigen, von Willebrand factor activity, and factor VIII levels also contributes to the atherosclerotic plaque. Decreased antiaggregatory prostacyclin production and enhanced proaggregatory thromboxane synthesis from activated platelets can tilt the homeostatic situation towards a prothrombotic and proinflammatory phenotype in endothelial cells [35–37].

4. COVID-19 in Renal Disease Patients

Kidney disease is defined as an impaired glomerular filtration rate (GFR) or structural abnormalities as measured by albuminuria or abnormal urine analysis for 3 or more months [38]. The glomerulus is the filtration unit of the kidney, and an increase permeability of albumin is an early sign of renal dysfunction and kidney disease. It is a well-known fact that hypertension [16] and diabetes [39] promote kidney injury and contribute to renal failure particularly in elderly patients [40] and could predispose these individuals to COVID-19 infection. Recent systemic reviews and meta-analysis of the COVID-19 patients revealed that the prevalence of chronic kidney disease (CKD) was 9.1% worldwide [40–42] and about 15% in the United States of America [43]. A meta-analysis from Fisher et.al. showed that about 20% of patients with kidney disease and comorbidity had a 3-fold higher risk of contracting viral infection than those without CKD. Furthermore, patients with acute kidney injury (AKI) who tested positive for COVID-19 had a higher risk of CKD [44] than those who did not have AKI [45], recognizing CKD plays a key role in the severity of COVID-19.

The kidney is a likely target for COVID-19 due to its high number of cellular ACE2 receptors. These receptors are mainly localized in the glomerulus, mesangial cells, podocytes, and distal nephron [46–48] As discussed earlier, ACE2 is counterregulatory to local and systemic RAAS; therefore, decrease in ACE2 increases ang II accumulation and promotes albuminuria [46] suggesting its role in glomerular permeability. Additionally, protein efflux could be due to upregulation of angiotensin II receptor type 1 (AT1R) and prorenin receptor- (PRR-) activating proinflammatory pathways via the Wnt-catenin-snail pathway causing podocyte injury and actin rearrangement [49]. In hypertension and renal disease, it is shown that ACE2 expression is decreased promoting glomerular hypertrophy and proteinuria [50]. In diabetic kidney disease, ACE2 expression was found to be significantly decreased resulting in the formation of reactive oxygen species, kidney fibrosis, collagen deposition, mesangial matrix expansion, and podocyte loss [51]. This evidence indicates that disruption of RAAS homeostasis via downregulation of ACE2 and increase in ACE/ang II/AT1R activity impairs renal function and contributes to the COVID-19 infection, hospitalization, and mortality.

5. Management of Cardiorenal Complications in COVID-19 Patients

COVID-19 patients have higher levels of inflammatory cytokines. Both intensive care unit (ICU) patients and non-ICU patients with SARS-CoV-2 infection reported significantly higher plasma concentrations of interleukins and other cytokines than healthy subjects [34]. In cardiorenal diseases, ang II is responsible for cell proliferation, fibrosis, and hypertrophy by acting as a vasoconstrictor, proinflammatory, and prooxidative hormone which increases salt and water retention [16, 52] leading to end-organ dysfunction. RAAS blockers such as angiotensin-converting enzyme inhibitors (ACEI) and angiotensin receptor blockers (ARBs) are the most commonly used drugs in patients with hypertension, heart failure, and chronic kidney disease as they provide end-organ protection and increase ACE2 expression responsible for vasodilatory effects [53, 54]. Due to concerns that elevated ACE2 expression facilitates SARS-CoV-2 infection, the theory of a negative impact of RAAS inhibitors gained popularity early in the pandemic [55]. However, recent studies have challenged those theories and showed that the RAAS inhibitors can be safely used in COVID-19 patients with cardiorenal comorbidities [56].

Review of the literature and a recent meta-analysis of 52 studies with more than 10000 patients contributes to a growing body of evidence indicating that the ACE-I/ARBs do not harm COVID-19 patients and in fact provide protective benefits by controlling the blood pressure which lowers the risk of mortality [57]. Another study comprising of more than 17000 COVID-19 patients reported that the ACE-I/ARBs decrease the need of ICU admission, mechanical ventilation, and progression of critical pneumonia with multiple mixed comorbidities [58]. Taken together, these studies indicates that the RAAS antagonist plays a protective role in COVID-19 across all patient groups. Patients who take other blood pressure medications have shown poorer clinical outcomes and are more likely to have significant adverse effects than those who take ACE-I/ARBs. As a result, the international scientific community including American Heart Association recommends that COVID-19 individuals with metabolic syndrome receive ACE-I/ARBs unless contraindicated.

ACE-I/ARBs mediate its cardiorenal protective effects by inhibiting fibrosis and inflammation. Research have proved that ACE-I/ARBs decrease proinflammatory markers including IL-6, IL-1β, MCP-1, NF-κB, TNF-α, C-reactive protein, intracellular adhesion molecule-1, and vascular adhesion molecule-1 [59, 60]. These effects could in part due to unopposed activation of angiotensin type 2 receptor (AT2R) and increase in expression of inhibitory kappa B [61].

There are certain limitations to this review, because research with higher levels of evidence, such as randomized clinical trials, were unavailable.

6. Conclusion

COVID-19 patients frequently have cardiorenal comorbidities, putting them at a higher risk of morbidity and mortality. The use of a clinically approved RAAS antagonist should be continued, according to the available data. Although this study emphasizes the link between RAAS inhibitors and mortality in COVID-19 patients, further randomized trials are required to demonstrate correlation.

Conflicts of Interest

The author declares no conflicts of interest in this work.

Authors’ Contributions

All authors made an equal contribution to the review article and read and approved the final version to be published.

Acknowledgments

This article was supported by the DeBusk College of Osteopathic Medicine, Lincoln Memorial University.

References

University JH, “Coronavirus resource center COVID-19 dashboard by the Center for Systems Science and Engineering (CSSE) at Johns Hopkins University (JHU),” February 2022, https://coronavirus.jhu.edu/map.html.
View at: Google Scholar
Z. Wu and J. M. McGoogan, “Characteristics of and important lessons from the coronavirus disease 2019 (COVID-19) outbreak in China,” JAMA, vol. 323, no. 13, pp. 1239–1242, 2020.
View at: Publisher Site | Google Scholar
J. Powell and C. R. Piszczatoski, “Finally, an FDA approval for an immunization against COVID-19: hope on the horizon,” Annals of Pharmacotherapy, vol. 10, p. 10600280211058387, 2022.
View at: Publisher Site | Google Scholar
D. Vasireddy, P. Atluri, S. V. Malayala, R. Vanaparthy, and G. Mohan, “Review of COVID-19 vaccines approved in the United States of America for emergency use,” Journal of Clinical Medical Research, vol. 13, no. 4, pp. 204–213, 2021.
View at: Publisher Site | Google Scholar
B. J. Bosch, R. van der Zee, C. A. de Haan, and P. J. Rottier, “The coronavirus spike protein is a class I virus fusion protein: structural and functional characterization of the fusion core complex,” Journal of Virology, vol. 77, no. 16, pp. 8801–8811, 2003.
View at: Publisher Site | Google Scholar
M. Hoffmann, H. Kleine-Weber, S. Schroeder et al., “SARS-CoV-2 cell entry depends on ACE2 and TMPRSS2 and is blocked by a clinically proven protease inhibitor,” Cell, vol. 181, no. 2, pp. 271–280.e8, 2020.
View at: Publisher Site | Google Scholar
A. C. Walls, Y. J. Park, M. A. Tortorici, A. Wall, A. T. McGuire, and D. Veesler, “Structure, function, and antigenicity of the SARS-CoV-2 spike glycoprotein,” Cell, vol. 181, no. 2, pp. 281–292.e6, 2020.
View at: Publisher Site | Google Scholar
Y. Zhao, Z. Zhao, Y. Wang, Y. Zhou, Y. Ma, and W. Zuo, “Single-cell RNA expression profiling of ACE2, the receptor of SARS-CoV-2,” American Journal of Respiratory and Critical Care Medicine, vol. 202, no. 5, pp. 756–759, 2020.
View at: Publisher Site | Google Scholar
H. Zhang, J. M. Penninger, Y. Li, N. Zhong, and A. S. Slutsky, “Angiotensin-converting enzyme 2 (ACE2) as a SARS-CoV-2 receptor: molecular mechanisms and potential therapeutic target,” Intensive Care Medicine, vol. 46, no. 4, pp. 586–590, 2020.
View at: Publisher Site | Google Scholar
S. Ghoneim, M. U. Butt, O. Hamid, A. Shah, and I. Asaad, “The incidence of COVID-19 in patients with metabolic syndrome and non- alcoholic steatohepatitis: A population-based study,” Metabolism Open, vol. 8, article 100057, 2020.
View at: Publisher Site | Google Scholar
A. Badawi and S. G. Ryoo, “Prevalence of comorbidities in the Middle East respiratory syndrome coronavirus (MERS-CoV): a systematic review and meta-analysis,” International Journal of Infectious Diseases, vol. 49, pp. 129–133, 2016.
View at: Publisher Site | Google Scholar
A. Mascolo, C. Scavone, C. Rafaniello et al., “The role of renin-angiotensin-aldosterone system in the heart and lung: focus on COVID-19,” Frontiers in Pharmacology, vol. 12, article 667254, 2021.
View at: Publisher Site | Google Scholar
G. Yang, Z. Tan, L. Zhou et al., “Effects of angiotensin II receptor blockers and ACE (angiotensin-converting enzyme) inhibitors on virus infection, inflammatory status, and clinical outcomes in patients with COVID-19 and hypertension: a single-center retrospective study,” Hypertension, vol. 76, no. 1, pp. 51–58, 2020.
View at: Publisher Site | Google Scholar
M. Bansal, “Cardiovascular disease and COVID-19,” Diabetes and Metabolic Syndrome: Clinical Research and Reviews, vol. 14, no. 3, pp. 247–250, 2020.
View at: Publisher Site | Google Scholar
R. M. Carey and J. G. Wang, “Evidence that renin-angiotensin system inhibitors should not be discontinued due to the COVID-19 pandemic,” Hypertension, vol. 76, no. 1, pp. 42-43, 2020.
View at: Publisher Site | Google Scholar
S. S. Quadri, S. A. Culver, C. Li, and H. M. Siragy, “Interaction of the renin angiotensin and cox systems in the kidney,” Frontiers in Bioscience, vol. 8, no. 2, pp. 215–226, 2016.
View at: Publisher Site | Google Scholar
S. S. Quadri, C. Cooper, D. Ghaffar, H. Vaishnav, and L. Nahar, “The pathological role of pro (renin) receptor in renal inflammation,” Journal of Experimental Pharmacology, vol. 13, pp. 339–344, 2021.
View at: Publisher Site | Google Scholar
A. Mascolo, M. Sessa, C. Scavone et al., “New and old roles of the peripheral and brain renin-angiotensin-aldosterone system (RAAS): focus on cardiovascular and neurological diseases,” International Journal of Cardiology, vol. 227, pp. 734–742, 2017.
View at: Publisher Site | Google Scholar
R. S. Padda, Y. Shi, C. S. Lo, S. L. Zhang, and J. S. Chan, “Angiotensin-(1-7): a novel peptide to treat hypertension and nephropathy in diabetes?” Journal of Diabetes & Metabolism, vol. 6, no. 10, 2015.
View at: Publisher Site | Google Scholar
A. J. Turner, J. A. Hiscox, and N. M. Hooper, “ACE2: from vasopeptidase to SARS virus receptor,” Trends in Pharmacological Sciences, vol. 25, no. 6, pp. 291–294, 2004.
View at: Publisher Site | Google Scholar
Y. Y. Zheng, Y. T. Ma, J. Y. Zhang, and X. Xie, “COVID-19 and the cardiovascular system,” Nature Reviews Cardiology, vol. 17, no. 5, pp. 259-260, 2020.
View at: Publisher Site | Google Scholar
F. Zhou, T. Yu, R. Du et al., “Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: a retrospective cohort study,” Lancet, vol. 395, no. 10229, pp. 1054–1062, 2020.
View at: Publisher Site | Google Scholar
N. R. Barbaro, V. Fontana, R. Modolo et al., “Increased arterial stiffness in resistant hypertension is associated with inflammatory biomarkers,” Blood Pressure, vol. 24, no. 1, pp. 7–13, 2015.
View at: Publisher Site | Google Scholar
R. M. Inciardi, L. Lupi, G. Zaccone et al., “Cardiac involvement in a patient with coronavirus disease 2019 (COVID-19),” JAMA Cardiology, vol. 5, no. 7, pp. 819–824, 2020.
View at: Publisher Site | Google Scholar
G. Y. Oudit, Z. Kassiri, C. Jiang et al., “SARS-coronavirus modulation of myocardial ACE2 expression and inflammation in patients with SARS,” European Journal of Clinical Investigation, vol. 39, no. 7, pp. 618–625, 2009.
View at: Publisher Site | Google Scholar
H. Hu, F. Ma, X. Wei, and Y. Fang, “Coronavirus fulminant myocarditis treated with glucocorticoid and human immunoglobulin,” European Heart Journal, vol. 42, no. 2, p. 206, 2021.
View at: Publisher Site | Google Scholar
J. Yang, Y. Zheng, X. Gou et al., “Prevalence of comorbidities and its effects in patients infected with SARS- CoV-2: a systematic review and meta-analysis,” International Journal of Infectious Diseases, vol. 94, pp. 91–95, 2020.
View at: Publisher Site | Google Scholar
T. Guo, Y. Fan, M. Chen et al., “Cardiovascular implications of fatal outcomes of patients with coronavirus disease 2019 (COVID-19),” JAMA Cardiology, vol. 5, no. 7, pp. 811–818, 2020.
View at: Publisher Site | Google Scholar
P. M. Moriarty, L. K. Gorby, E. S. Stroes, J. P. Kastelein, M. Davidson, and S. Tsimikas, “Lipoprotein (a) and its potential association with thrombosis and inflammation in COVID-19: a testable hypothesis,” Current Atherosclerosis Reports, vol. 22, no. 9, p. 48, 2020.
View at: Publisher Site | Google Scholar
Y. Belkaid and B. T. Rouse, “Natural regulatory T cells in infectious disease,” Nature Immunology, vol. 6, no. 4, pp. 353–360, 2005.
View at: Publisher Site | Google Scholar
C. Qin, L. Zhou, Z. Hu et al., “Dysregulation of immune response in patients with coronavirus 2019 (COVID-19) in Wuhan, China,” Clinical Infectious Diseases, vol. 71, no. 15, pp. 762–768, 2020.
View at: Publisher Site | Google Scholar
A. Shimabukuro-Vornhagen, P. Gödel, M. Subklewe et al., “Cytokine release syndrome,” Journal for Immunotherapy of Cancer, vol. 6, no. 1, p. 56, 2018.
View at: Publisher Site | Google Scholar
J. R. Tisoncik, M. J. Korth, C. P. Simmons, J. Farrar, T. R. Martin, and M. G. Katze, “Into the eye of the cytokine storm,” Microbiology and Molecular Biology Reviews, vol. 76, no. 1, pp. 16–32, 2012.
View at: Publisher Site | Google Scholar
C. Huang, Y. Wang, X. Li et al., “Clinical features of patients infected with 2019 Novel coronavirus in Wuhan, China,” Lancet, vol. 395, no. 10223, pp. 497–506, 2020.
View at: Publisher Site | Google Scholar
M. H. Petri, C. Tellier, C. Michiels, I. Ellertsen, J. M. Dogne, and M. Back, “Effects of the dual TP receptor antagonist and thromboxane synthase inhibitor EV-077 on human endothelial and vascular smooth muscle cells,” Biochemical and Biophysical Research Communications, vol. 441, no. 2, pp. 393–398, 2013.
View at: Publisher Site | Google Scholar
S. P. Tull, S. I. Anderson, S. C. Hughan, S. P. Watson, G. B. Nash, and G. E. Rainger, “Cellular pathology of Atherosclerosis,” Circulation Research, vol. 98, no. 1, pp. 98–104, 2006.
View at: Publisher Site | Google Scholar
M. Chimen, A. Evryviadou, C. L. Box et al., “Appropriation of GPIbα from platelet-derived extracellular vesicles supports monocyte recruitment in systemic inflammation,” Haematologica, vol. 105, no. 5, pp. 1248–1261, 2020.
View at: Publisher Site | Google Scholar
Council E-E, Group EW, “Chronic kidney disease is a key risk factor for severe COVID-19: a call to action by the ERA-EDTA,” Nephrology, Dialysis, Transplantation, vol. 36, no. 1, pp. 87–94, 2021.
View at: Publisher Site | Google Scholar
C. Li and H. M. Siragy, “Autophagy upregulates (pro) renin receptor expression via reduction of P 62/SQSTM1 and activation of ERK1/2 signaling pathway in podocytes,” American Journal of Physiology. Regulatory, Integrative and Comparative Physiology, vol. 313, no. 1, pp. R58–R64, 2017.
View at: Publisher Site | Google Scholar
S. K. Kunutsor and J. A. Laukkanen, “Renal complications in COVID-19: a systematic review and meta-analysis,” Annals of Medicine, vol. 52, no. 7, pp. 345–353, 2020.
View at: Publisher Site | Google Scholar
K. Nandy, A. Salunke, S. K. Pathak et al., “Coronavirus disease (COVID-19): a systematic review and meta-analysis to evaluate the impact of various comorbidities on serious events,” Diabetes and Metabolic Syndrome: Clinical Research and Reviews, vol. 14, no. 5, pp. 1017–1025, 2020.
View at: Publisher Site | Google Scholar
Collaboration GBDCKD, “Global, regional, and national burden of chronic kidney disease, 1990-2017: a systematic analysis for the global burden of disease study 2017,” Lancet, vol. 395, no. 10225, pp. 709–733, 2020.
View at: Publisher Site | Google Scholar
S. Richardson, J. S. Hirsch, M. Narasimhan et al., “Presenting characteristics, comorbidities, and outcomes among 5700 patients hospitalized with COVID-19 in the new York City area,” JAMA, vol. 323, no. 20, pp. 2052–2059, 2020.
View at: Publisher Site | Google Scholar
S. S. Jdiaa, R. Mansour, A. El Alayli, A. Gautam, P. Thomas, and R. A. Mustafa, “COVID-19 and chronic kidney disease: an updated overview of reviews,” Journal of Nephrology, vol. 35, no. 1, pp. 69–85, 2022.
View at: Publisher Site | Google Scholar
M. Fisher, J. Neugarten, E. Bellin et al., “AKI in hospitalized patients with and without COVID-19: a comparison study,” Journal of the American Society of Nephrology, vol. 31, no. 9, pp. 2145–2157, 2020.
View at: Publisher Site | Google Scholar
M. Ye, J. Wysocki, J. William, M. J. Soler, I. Cokic, and D. Batlle, “Glomerular localization and expression of angiotensin-converting enzyme 2 and angiotensin-converting enzyme: implications for albuminuria in diabetes,” Journal of the American Society of Nephrology, vol. 17, no. 11, pp. 3067–3075, 2006.
View at: Publisher Site | Google Scholar
K. Kuba, Y. Imai, S. Rao et al., “A crucial role of angiotensin converting enzyme 2 (ACE2) in SARS coronavirus-induced lung injury,” Nature Medicine, vol. 11, no. 8, pp. 875–879, 2005.
View at: Google Scholar
A. Emami, F. Javanmardi, N. Pirbonyeh, and A. Akbari, “Prevalence of underlying diseases in hospitalized patients with COVID-19: a systematic review and meta-analysis,” Archives of Academic Emergency Medicine, vol. 8, no. 1, article e35, 2020.
View at: Google Scholar
G. Wolf, S. Chen, and F. N. Ziyadeh, “From the periphery of the glomerular capillary wall toward the center of disease: podocyte injury comes of age in diabetic nephropathy,” Diabetes, vol. 54, no. 6, pp. 1626–1634, 2005.
View at: Google Scholar
R. C. Berger, P. F. Vassallo, O. Crajoinas Rde et al., “Renal effects and underlying molecular mechanisms of long-term salt content diets in spontaneously hypertensive rats,” PLoS One, vol. 10, no. 10, article e0141288, 2015.
View at: Publisher Site | Google Scholar
J. Wysocki, M. Ye, A. M. Khattab et al., “Angiotensin-converting enzyme 2 amplification limited to the circulation does not protect mice from development of diabetic nephropathy,” Kidney International, vol. 91, no. 6, pp. 1336–1346, 2017.
View at: Publisher Site | Google Scholar
S. Culver, C. Li, and H. M. Siragy, “Intrarenal angiotensin-converting enzyme: the old and the new,” Current Hypertension Reports, vol. 19, no. 10, p. 80, 2017.
View at: Publisher Site | Google Scholar
M. J. Soler, C. Barrios, R. Oliva, and D. Batlle, “Pharmacologic modulation of ACE2 expression,” Current Hypertension Reports, vol. 10, no. 5, pp. 410–414, 2008.
View at: Publisher Site | Google Scholar
C. M. Ferrario, J. Jessup, M. C. Chappell et al., “Effect of angiotensin-converting enzyme inhibition and angiotensin II receptor blockers on cardiac angiotensin-converting enzyme 2,” Circulation, vol. 111, no. 20, pp. 2605–2610, 2005.
View at: Publisher Site | Google Scholar
R. M. Touyz, H. Li, and C. Delles, “ACE2 the Janus-faced protein - from cardiovascular protection to severe acute respiratory syndrome-coronavirus and COVID-19,” Clinical Science, vol. 134, no. 7, pp. 747–750, 2020.
View at: Publisher Site | Google Scholar
H. R. Reynolds, S. Adhikari, C. Pulgarin et al., “Renin-angiotensin-aldosterone system inhibitors and risk of COVID-19,” The New England Journal of Medicine, vol. 382, no. 25, pp. 2441–2448, 2020.
View at: Publisher Site | Google Scholar
R. Baral, V. Tsampasian, M. Debski et al., “Association between renin-angiotensin-aldosterone system inhibitors and clinical outcomes in patients with COVID-19: a systematic review and meta-analysis,” JAMA Network Open, vol. 4, no. 3, article e213594, 2021.
View at: Publisher Site | Google Scholar
J. Barochiner and R. Martinez, “Use of inhibitors of the renin-angiotensin system in hypertensive patients and COVID-19 severity: a systematic review and meta-analysis,” Journal of Clinical Pharmacy and Therapeutics, vol. 45, no. 6, pp. 1244–1252, 2020.
View at: Publisher Site | Google Scholar
P. Dandona, S. Dhindsa, H. Ghanim, and A. Chaudhuri, “Angiotensin II and inflammation: the effect of angiotensin-converting enzyme inhibition and angiotensin II receptor blockade,” Journal of Human Hypertension, vol. 21, no. 1, pp. 20–27, 2007.
View at: Publisher Site | Google Scholar
C. M. Ferrario and W. B. Strawn, “Role of the renin-angiotensin-aldosterone system and proinflammatory mediators in cardiovascular disease,” The American Journal of Cardiology, vol. 98, no. 1, pp. 121–128, 2006.
View at: Publisher Site | Google Scholar
L. C. Matavelli and H. M. Siragy, “AT2 receptor activities and pathophysiological implications,” Journal of Cardiovascular Pharmacology, vol. 65, no. 3, pp. 226–232, 2015.
View at: Publisher Site | Google Scholar

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Copyright © 2022 Muhtasham Sifaat et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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