Vascular endothelial cadherin shedding is more severe in sepsis patients with severe acute kidney injury View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2019-12

AUTHORS

Wen-Kuang Yu, J. Brennan McNeil, Nancy E. Wickersham, Ciara M. Shaver, Julie A. Bastarache, Lorraine B. Ware

ABSTRACT

BACKGROUND: Vascular endothelial cadherin (VE-cadherin) is a membrane protein that is the major component of adherens junctions between endothelial cells. It is crucial for regulating vascular integrity, endothelial permeability, and angiogenesis. During inflammatory processes, VE-cadherin is shed into circulation (sVE-cadherin). Plasma sVE-cadherin is elevated in sepsis, malignancy, autoimmune diseases, and coronary atherosclerosis. However, the relationship between specific organ failures, especially severe acute kidney injury (AKI) defined by requirement for renal replacement therapy (AKI-RRT), and plasma sVE-cadherin levels in severe sepsis has not been well studied. METHODS: The present study is a prospective study of critically ill adults with sepsis and acute respiratory failure (age ≥ 18 years) enrolled in the Validating Acute Lung Injury markers for Diagnosis (VALID) study. Plasma sVE-cadherin was measured at study enrollment. Primary analysis focused on the association between sVE-cadherin levels and the development of AKI, AKI-RRT, other organ dysfunction as defined by Brussels organ failure scores, pulmonary versus non-pulmonary sepsis, acute respiratory distress syndrome (ARDS), and in-hospital mortality. RESULTS: Of 228 severe sepsis patients included, 80 (35%) developed AKI-RRT. Plasma sVE-cadherin levels at enrollment were significantly higher in patients with AKI-RRT compared with patients without AKI-RRT (p = 0.003). Plasma sVE-cadherin levels by quartile were significantly higher in severe sepsis patients with acute kidney injury stage 3 (p = 0.044) as defined by Kidney Disease Improving Global Outcomes (KDIGO) criteria. Patients with greater than 2 organ failures had higher plasma sVE-cadherin levels than patients with 2 or fewer organ failures (p < 0.001). In a multivariable analysis, plasma sVE-cadherin was independently associated with AKI-RRT (odds ratio 6.44 per log increase in plasma sVE-cadherin, 95% CI 1.126-36.847, p = 0.036). Plasma sVE-cadherin levels were significantly higher in patients with non-pulmonary sepsis compared to pulmonary sepsis (p < 0.001). CONCLUSION: Shedding of sVE-cadherin is associated with severe acute kidney injury and with more severe organ dysfunction in patients with sepsis, suggesting that breakdown of endothelial adherens junctions may contribute to the pathogenesis of organ dysfunction in sepsis. Further studies of sVE-cadherin as a biomarker of disease severity in clinical sepsis are needed to better elucidate the role of VE-cadherin shedding in sepsis-induced severe organ dysfunction. More... »

PAGES

18

Identifiers

URI

http://scigraph.springernature.com/pub.10.1186/s13054-019-2315-y

DOI

http://dx.doi.org/10.1186/s13054-019-2315-y

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1111508786

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/30658667


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244 Division of Allergy, Pulmonary, and Critical Care Medicine, Department of Medicine, Vanderbilt University Medical Center, T1218 MCN, 1161 21st, Avenue S, 37232, Nashville, TN, USA
245 rdf:type schema:Organization
246 https://www.grid.ac/institutes/grid.412807.8 schema:alternateName Vanderbilt University Medical Center
247 schema:name Division of Allergy, Pulmonary, and Critical Care Medicine, Department of Medicine, Vanderbilt University Medical Center, T1218 MCN, 1161 21st, Avenue S, 37232, Nashville, TN, USA
248 Division of Respiratory Therapy, Department of Chest Medicine, Taipei Veterans General Hospital, No. 201, Sec. 2, Shipai Rd., Beitou District, 11217, Taipei City, Taiwan, Republic of China
249 Institute of Physiology, National Yang-Ming University, Taipei, Taiwan
250 rdf:type schema:Organization
 




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