The curse of angiopoietin-2 in ARDS: on stranger TI(E)des

Kümpers, Philipp; Lukasz, Alexander

doi:10.1186/s13054-018-1978-0

Cited by 15 publications

(13 citation statements)

References 34 publications

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“…Angiopoietin-2 was significantly higher in non-survivors ( n = 10) and a quite similar cut-off of 4.0 ng/mL predicted ICU mortality with a sensitivity of 89% and a specificity of 77%. Interestingly, the levels of the protective angiopoietin-1 were the same in both groups, a finding that is consistent with two other reports [ 75 , 94 ] and many previous studies on ARDS in bacterial sepsis [ 96 ]. Bermejo-Martin et al analyzed the viral RNA load of SARS-CoV-2 (RNAemia) in plasma samples of 250 COVID-19 patients (50 outpatients, 100 hospitalized ward patients and 100 critically ill).…”

Section: Covid-19 Is An Endothelial Diseasesupporting

confidence: 92%

COVID-19 is a systemic vascular hemopathy: insight for mechanistic and clinical aspects

et al. 2021

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Coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is presenting as a systemic disease associated with vascular inflammation and endothelial injury. Severe forms of SARS-CoV-2 infection induce acute respiratory distress syndrome (ARDS) and there is still an ongoing debate on whether COVID-19 ARDS and its perfusion defect differs from ARDS induced by other causes. Beside pro-inflammatory cytokines (such as interleukin-1 β [IL-1β] or IL-6), several main pathological phenomena have been seen because of endothelial cell (EC) dysfunction: hypercoagulation reflected by fibrin degradation products called D-dimers, micro- and macrothrombosis and pathological angiogenesis. Direct endothelial infection by SARS-CoV-2 is not likely to occur and ACE-2 expression by EC is a matter of debate. Indeed, endothelial damage reported in severely ill patients with COVID-19 could be more likely secondary to infection of neighboring cells and/or a consequence of inflammation. Endotheliopathy could give rise to hypercoagulation by alteration in the levels of different factors such as von Willebrand factor. Other than thrombotic events, pathological angiogenesis is among the recent findings. Overexpression of different proangiogenic factors such as vascular endothelial growth factor (VEGF), basic fibroblast growth factor (FGF-2) or placental growth factors (PlGF) have been found in plasma or lung biopsies of COVID-19 patients. Finally, SARS-CoV-2 infection induces an emergency myelopoiesis associated to deregulated immunity and mobilization of endothelial progenitor cells, leading to features of acquired hematological malignancies or cardiovascular disease, which are discussed in this review. Altogether, this review will try to elucidate the pathophysiology of thrombotic complications, pathological angiogenesis and EC dysfunction, allowing better insight in new targets and antithrombotic protocols to better address vascular system dysfunction. Since treating SARS-CoV-2 infection and its potential long-term effects involves targeting the vascular compartment and/or mobilization of immature immune cells, we propose to define COVID-19 and its complications as a systemic vascular acquired hemopathy.

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Section: Covid-19 Is An Endothelial Diseasesupporting

confidence: 92%

COVID-19 is a systemic vascular hemopathy: insight for mechanistic and clinical aspects

et al. 2021

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“…In humans, sepsis and shock development are associated with higher plasma levels of AGPT2 . In acute respiratory distress syndrome (ARDS), AGPT2 is one of the most promising severity biomarkers and it has been implicated in ARDS pathogenesis …”

Section: Introductionmentioning

confidence: 99%

Angiopoietin‐2 as a predictor of acute kidney injury in critically ill patients and association with ARDS

et al. 2019

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Background and objective Angiopoietin‐2 (AGPT2) has been proposed as a key mediator of organ dysfunction, mainly in acute respiratory distress syndrome (ARDS). It has also been associated with acute kidney injury (AKI). We aimed to investigate the role of AGPT2 in patients with and without ARDS. Methods In a cohort study with critically ill patients, AGPT1 and AGPT2 were assayed in plasma collected within the first 24 h after admission to intensive care unit (ICU). Severe AKI and the need for dialysis were outcome measures from comparative analysis with clinical characteristics useful for AKI risk stratification. Results Among 283 patients (50.2% males), 109 (38.5%) had ARDS. AGPT2 levels at admission were higher in patients with ARDS. Although overall AGPT2 and AGPT2/AGPT1 levels were associated with severe AKI, this association was not significant in patients without ARDS; however, it remained strongly significant in ARDS patients. In patients without ARDS, AGPT2 showed only a weak discriminatory capacity to predict severe AKI (area under the curve (AUC): 0.64 vs 0.81 in the ARDS group). The continuous net reclassification improvement (NRI) in the ARDS group resulting from AGPT2 inclusion was 64.1% (P < 0.001) and the integrated discrimination improvement (IDI) index was 0.057 (P = 0.003). There was no significant difference in NRI in the no‐ARDS group. Conclusion AGPT2 and AGPT2/AGPT1 ratio are associated with severe AKI and there was only a need of renal replacement therapy (RRT) in patients with or at risk of ARDS, not in other critically ill patients. Adding AGPT2 to a clinical model resulted in a significant improvement in the capacity to predict severe AKI specifically in ARDS patients.

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“…Angiopoietin-2 levels are increased in patients with ARDS and sepsis and are associated with worse outcomes (111)(112)(113)(114). An angiopoietin-1 mimetic and angiopoietin-2-binding antibodies have been shown to prevent lung injury in preclinical ARDS (115) and sepsis (116) models and are currently being developed for possible use in patients with ARDS (117).…”

Section: Resolution and Repair Of Injurymentioning

confidence: 99%

Integrating molecular pathogenesis and clinical translation in sepsis-induced acute respiratory distress syndrome

2019

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The curse of angiopoietin-2 in ARDS: on stranger TI(E)des

Cited by 15 publications

References 34 publications

COVID-19 is a systemic vascular hemopathy: insight for mechanistic and clinical aspects

COVID-19 is a systemic vascular hemopathy: insight for mechanistic and clinical aspects

Angiopoietin‐2 as a predictor of acute kidney injury in critically ill patients and association with ARDS

Integrating molecular pathogenesis and clinical translation in sepsis-induced acute respiratory distress syndrome

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