Acute kidney injury is associated with increased levels of circulating microvesicles in patients with decompensated cirrhosis. Issue 7 (July 2021)

• Record Type: Journal Article
• Authors: Campello, Elena; Zanetto, Alberto; Radu, Claudia M.; Bulato, Cristiana; Truma, Addolorata; Spiezia, Luca; Senzolo, Marco; Garcia-Tsao, Guadalupe; Simioni, Paolo
• Is Part Of: Digestive and liver disease. Volume 53:Issue 7(2021)
• Page Start: 879
• Page End: 888
• Publication Date: 2021-07
• Subjects: Chronic liver disease -- Coagulopathy -- Endothelial dysfunction -- Inflammation -- Microparticles; MVs microvesicles -- EVs extra-cellular vesicles -- AKI acute kidney injury -- MELD model for end stage liver disease -- VH variceal hemorrhage -- ACLF acute on chronic liver failure -- CKD chronic kidney disease -- PPP platelet poor plasma -- VSSC violet side scatter SSC -- PE phycoerythrin -- ORs odds-ratios -- CI confidence interval; Digestive organs -- Diseases -- Periodicals; Liver -- Diseases -- Periodicals; 616.33005
• DOI: 10.1016/j.dld.2020.12.118
• Languages: English
• ISSNs: 1590-8658

Abstract

Abstract: Background: Microvesicles (MVs) play a role in inflammation, coagulation, and vascular homeostasis in liver disease. Aim: To characterize circulating plasma MVs profile in patients with decompensated cirrhosis and acute kidney injury (AKI). Methods: We measured the levels of total, endothelial, platelet, tissue factor (TF)+, leukocyte and hepatocyte MVs by new generation flow-cytometry in a prospective cohort of patients with decompensated cirrhosis with and without AKI. Results: Eighty patients with decompensated cirrhosis were recruited (40 each with and without AKI). Patients with cirrhosis with AKI had significantly higher calcein+ (total), endothelial, and platelet-MVs. Conversely, TF+, leukocyte, and hepatocyte-MVs were comparable between groups. Resolution of AKI was associated with significantly decreased total and endothelial-MVs that became comparable with those in patients without AKI. Platelet MVs significantly decreased but remained higher compared to patients without AKI. TF+MVs significantly decreased and became lower than patients without AKI. Leukocyte and hepatocyte-MVs remained unchanged. Creatinine (OR 4.3 [95%CI 1.8–10.7]), MELD (OR 1.13 [95%CI 1.02–1.27]), any bleeding (OR 9.07 [95%CI 2.02–40.6]), and hepatocyte-MVs (OR 1.04 [95%CI 1.02–1.07]) were independently associated with 30-day mortality. Conclusion: AKI worsened vascular and cellular homeostasis in patients with cirrhosis, particularly by inducing endothelial dysfunction and platelet activation. AKI did not worsen systemic inflammation and hepatocytes activation.