“…Secondly, in the current cohort, all the patients presented high in ammatory response to SARS-CoV-2 infection, including high levels of IL6 plasma concentrations, as documented in previous studies (30) and morevover those who developed AKI had signi cantly higher CRP and PCT values on ICU admission.…”
BackgroundThe new coronavirus (SARS-CoV-2) infection leads to 5% to 16% hospitalization in Intensive Care Units (ICU) and is associated with 23% to 75% of kidney impairments, including acute kidney injury (AKI), as a major prognosis factor. The current work aims to characterize the renal impairment associated to SARS-CoV-2 in ICU patients, to evaluate its risk factors and its relationship with morbidity and mortality. Methods Forty-two patients consecutively admitted to the ICU of a university hospital (Paris, France) who tested positive for SARS-CoV-2 between March 25, 2020 and April 29, 2020 were included and classified in categories according to their renal function. Complete renal profiles and their evolution during ICU stay were fully characterized in 34 patients. Factors associated with AKI were identified through univariate analysis.ResultsThirty-two patients (94,1%) met diagnostic criteria for intrinsic renal injury with a mixed pattern of tubular and glomerular injuries within the first week of ICU admission, that lasted upon discharge. During their ICU stay, 24 patients (57.1%) presented AKI which was associated with increased mortality (p = 0.007), hemodynamic failure (p = 0.022), and more altered clearance at hospital discharge (p = 0.001). AKI occurrence was associated with lower pH (p = 0.024), higher PaCO2 (p = 0.027), PEEP (p = 0.027), procalcitonin (p = 0.015), and CRP (p = 0.045) on ICU admission.ConclusionsCritical SARS-CoV-2 is associated with persistent intrinsic renal injury and AKI, which is a risk factor of mortality. Identifying SARS-CoV-2 patients at risk of AKI will help in modifying clinical practice in ICU. Trial registration In accordance with the French law on biomedical research, this study obtained the approval of an Institutional Review Board (“Comité d’Éthique de la Recherche en Anesthésie-Réanimation” under the reference IRB 00010254 ‐ 2020 ‐ 106). Patients were all informed of the possible use of their data in researches as well as their right and terms of objection. Data were collected and integrated anonymously into a secure database in accordance with the French CNIL MR-004 methodology (registration number 20200803123416).
“…Secondly, in the current cohort, all the patients presented high in ammatory response to SARS-CoV-2 infection, including high levels of IL6 plasma concentrations, as documented in previous studies (30) and morevover those who developed AKI had signi cantly higher CRP and PCT values on ICU admission.…”
BackgroundThe new coronavirus (SARS-CoV-2) infection leads to 5% to 16% hospitalization in Intensive Care Units (ICU) and is associated with 23% to 75% of kidney impairments, including acute kidney injury (AKI), as a major prognosis factor. The current work aims to characterize the renal impairment associated to SARS-CoV-2 in ICU patients, to evaluate its risk factors and its relationship with morbidity and mortality. Methods Forty-two patients consecutively admitted to the ICU of a university hospital (Paris, France) who tested positive for SARS-CoV-2 between March 25, 2020 and April 29, 2020 were included and classified in categories according to their renal function. Complete renal profiles and their evolution during ICU stay were fully characterized in 34 patients. Factors associated with AKI were identified through univariate analysis.ResultsThirty-two patients (94,1%) met diagnostic criteria for intrinsic renal injury with a mixed pattern of tubular and glomerular injuries within the first week of ICU admission, that lasted upon discharge. During their ICU stay, 24 patients (57.1%) presented AKI which was associated with increased mortality (p = 0.007), hemodynamic failure (p = 0.022), and more altered clearance at hospital discharge (p = 0.001). AKI occurrence was associated with lower pH (p = 0.024), higher PaCO2 (p = 0.027), PEEP (p = 0.027), procalcitonin (p = 0.015), and CRP (p = 0.045) on ICU admission.ConclusionsCritical SARS-CoV-2 is associated with persistent intrinsic renal injury and AKI, which is a risk factor of mortality. Identifying SARS-CoV-2 patients at risk of AKI will help in modifying clinical practice in ICU. Trial registration In accordance with the French law on biomedical research, this study obtained the approval of an Institutional Review Board (“Comité d’Éthique de la Recherche en Anesthésie-Réanimation” under the reference IRB 00010254 ‐ 2020 ‐ 106). Patients were all informed of the possible use of their data in researches as well as their right and terms of objection. Data were collected and integrated anonymously into a secure database in accordance with the French CNIL MR-004 methodology (registration number 20200803123416).
“…The virus is known to enter cells via the ACE2 receptor, and may potentially interfere with the renin-angiotensin system in ways that alter pulmonary vascular tone 12 . Although it is reported that later stages of the disease are characterized by downregulation of ACE2 and vasoconstriction (promoting ARDS) [12][13][14] , it is possible that earlier stages instead promote local vasodilation or impairment of HPV 5,15 flow is equal to the fraction of lung with impaired oxygen transport (Fshu:Finj = 1). Heterogeneous 162 perfusion may increase the risk for larger Fshu, especially when the injured region also receives more baseline perfusion (see Figure 2).…”
Early stages of the novel coronavirus disease (COVID-19) have been associated with ‘silent hypoxia’ and poor oxygenation despite relatively small fractions of afflicted lung. Although it has been speculated that such paradoxical findings may be explained by impairment of hypoxic pulmonary vasoconstriction in infected lungs regions, no studies have confirmed this hypothesis nor determined whether such extreme degrees of perfusion redistribution are physiologically plausible. Here, we present a mathematical model which provides evidence that the extreme amount of pulmonary shunt observed in patients with early COVID-19 is not plausible without hyperperfusion of the relatively small fraction of injured lung, with three-fold increases in regional perfusion to afflicted regions. Although underlying perfusion heterogeneity (e.g., due to gravity or pulmonary emboli) exacerbated existing shunt in the model, the reported severity of hypoxia in early COVID-19 patients could not be replicated without considerable reduction of vascular resistance in nonoxygenated regions.
“…AGII will also stimulate the secretion of other hormones such as aldosterone and vasopressin. 14 , 17 , 18 AGI is a product of angiotensinogen (amino-acid protein), that is secreted by the liver and metabolized by enzyme renin. 14 SARS-CoV-2 can binds with angiotensin-converting enzyme 2 (ACE2) receptor via spike glycoprotein on its cell membrane that allows the virus to gain access in the targeted human cells where it will intracellularly replicate and display its cytotoxic properties.…”
Section: The Association Between Severe Acute Respiratory Syndrome Comentioning
confidence: 99%
“…The infection caused by SARS-CoV-2 will be augmented due to an increase in the presence of ACE2, allowing greater viral infiltration and replication to occur ( Figure 4 ). 18 , 49 Multi-organ failure will follow, especially involving organs that contain abundant ACE2 such as lungs, heart, kidneys, and intestine. Figure 4 Interaction Between SARS-CoV-2, AGII, ACE2, and ACE in Lung-Kidney-Cross-Talk.…”
Section: Etiology Of Aki In Sars-cov-2 Patientsmentioning
confidence: 99%
“…The levels of AGII will be increased in SARS-CoV-2 infection that gives rise to the release of more inflammatory mediators and the recruitment of more immune cells. 18 Many of these inflammatory mediators are prothrombotic that predispose to the development of macro and micro-thrombosis. The elevated levels of circulating AGII and inflammatory mediators will activate the platelets and endothelial cells of the blood vessels to release tissue and clotting factors causing thrombosis.…”
Section: Etiology Of Aki In Sars-cov-2 Patientsmentioning
Coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Since it was first recognized in December 2019, it has resulted in the ongoing worldwide pandemic. Although acute hypoxic respiratory failure (AHRF) and acute respiratory distress syndrome (ARDS) are the main features of the disease, the involvement of other organs needs to be explored. There has been a growing concern regarding the association between acute kidney injury (AKI) and poor outcomes in SARS-CoV-2 patients. Based on current observational data, AKI is the 2
nd
most common cause of morbidity and mortality behind ARDS in SARS-CoV-2 patients. Angiotensin-converting enzyme 2 (ACE2) receptor has been shown to be the cornerstone of SARS-CoV-2 infection and possibly plays a significant role in the occurrence of renal injury. The pathogenesis of AKI is likely multifactorial that involves not only direct viral invasion but also dysregulated immune response in the form of cytokine storm, ischemia to kidneys, hypercoagulable state, and rhabdomyolysis, among others. We performed a literature search of the Pubmed and Google Scholar database from 1996 to 2020 using the following keywords: severe acute respiratory syndrome coronavirus 2, coronavirus disease 2019, angiotensin-converting enzyme 2 receptor, and acute kidney injury to find the most pertinent and highest-quality of evidence. Any cited references were reviewed to identify relevant literature. The purpose of this review is to discuss, explore, and summarize the relationship between AKI in SARS-CoV-2 patients, with a focus on its epidemiology, association with ACE2 receptors, and pathogenesis of AKI.
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