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IntroductionOne of the most severe complications of repair surgery for abdominal aortic aneurysms (AAA) is acute kidney injury (AKI). Acute kidney injury is an inflammatory process whose pathogenesis involves endothelial cells (EC). The aim of this study was to assess the dynamics of endothelium injury markers measured during elective AAA surgery which might confirm the inflammatory character of AKI.Material and methodsThe study group consisted of 14 patients with AAA. We measured plasma soluble forms of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), E-selectin, P-selectin as well as the levels of von Willebrand factor (vWF) before, during (including intra-abdominal vein levels before and after aortic clamp removal) and within 2 days after surgery.ResultsWe have found a biphasic response of ICAM-1, VCAM-1 and P-selectin with an initial fall and subsequent rise. However, only VCAM-1 changes were significant compared to its baseline value. The maximum decrease of VCAM-1 was observed in the renal vein 5 min after aortic clamp removal (335.42 ±129.63 ng/ml vs. 488.90 ±169.80 ng/ml baseline value, p < 0.05), and the highest rise 48 h after aortic clamp removal (721.46 ±333.99 vs. baseline, p < 0.05).ConclusionsVascular cell adhesion molecule-1 turned out to be the most sensitive indicator of EC injury and inflammatory status after AAA surgery. During AAA surgery, soluble forms of P-selectin, ICAM-1 and VCAM-1 demonstrate a biphasic response with an initial fall and subsequent rise. These soluble forms could have a modulatory effect on the development of inflammation.

INTROduCTION One of the most severe complications of repair surgery for abdominal aortic aneurysms (AAA) is acute kidney injury (AKI). Even small rises in serum creatinine after surgery are associated with increased mortality. ObjECTIvEs The aim of the study was to assess the dynamics of AKI after elective AAA surgery using novel markers. PATIENTs ANd mEThOds The study group consisted of 14 patients with AAA. We measured serum neutrophil gelatinase-associated lipocalin (NGAL) before, during (including intra-abdominal vein levels before and after removal of aortic clamp), and within 2 days after surgery. Moreover, we assessed urinary NGAL, interleukin 18 (IL-18), and liver-type fatty acid-binding protein (L-FABP) before, during, and within 3 days after surgery. REsuLTs We observed a marked but nonsignificant increase in serum NGAL directly after clamp removal (75.21 ±55.83 vs. 46.37 ±21.60 ng/ml baseline value, P >0.05) and significantly elevated plasma NGAL at 2 hours (91.54 ±76.54 vs. baseline, P <0.05), 12 hours (100.78 ±44.92 vs. baseline, P <0.05) and 24 hours (89.46 ±94.18 vs. baseline, P <0.05) after clamp release. There was also significant elevation of urinary IL-18 at 2 hours (51.60 [12.12-527.16] vs. 25.99 [9.34-187.80] pg/ml at baseline, P <0.05); L-FABP at 2 hours (47.10 [5.40-500.00] vs. 5.50 (2.20-27.20) ng/ml at baseline, P <0.05) and 12 hours (39.00 [5.20-500.00] vs. baseline, P <0.05); NGAL at 12 hours (20.75 [5.00-176.10] vs. 5.85 [1.40-16.00] ng/ml at baseline, P <0.05) and 24 hours (13.95 [3.90-163.30] vs. baseline, P <0.05) after clamp release. CONCLusIONs Elective AAA surgery may induce AKI. Novel markers can facilitate early detection of AKI, thus allowing to start therapy at an appropriate time point.

Introduction Anticoagulant therapy in individuals with cirrhosis is challenging, as their risk of hemorrhage is significant due to concomitant alterations in primary hemostasis, secondary hemostasis and fibrinolysis. For many years, warfarin and heparin (including low molecular weight heparin) were the only treatment options for patients with thrombosis. Since 2010, novel, direct-acting oral anticoagulants (DOAC) that inhibit either thrombin (dabigatran) or factor Xa (e.g., rivaroxaban, apixaban, edoxaban, and betrixaban) are available. These direct-acting oral anticoagulants do not require laboratory monitoring and have minimal food and drug interactions, which makes them appealing to use for many patients. Unfortunately, there is inadequate data about efficacy and safety of these direct oral anticoagulants in cirrhotic patients as this group was commonly excluded from clinical trials evaluating these medications. In our study we aim to describe a large single institution experience with use of DOACs in patients with cirrhosis and explore clinical characteristics as potential predictors for bleeding and thrombosis. Methods: We conducted a retrospective cohort study of patients with cirrhosis who were seen in our institution between September 1, 2010 and June 30, 2017 and were treated with a DOAC utilizing a database search tool, called the Advanced Cohort Explorer that allows electronic records to be reviewed in a time efficient manner through text search or code search functionality. Only patients with cirrhosis diagnosed by histopathologic evaluation or with clinical presentation consistent with cirrhosis and confirmed by a gastroenterologist or by radiologic imaging (MRI, CT) were included in the study. Results: In our study, 106 individuals (male=72) met the inclusion criteria. Ninety three (88%) patients were treated with an anti-Xa inhibitor (rivaroxaban or apixaban), and remaining 13 (12%) with direct thrombin inhibitor (dabigatran). Median age at starting anticoagulant was 66 (range 24-89) years. The most common indication for anticoagulation was atrial fibrillation/flutter (54%), followed by pulmonary embolism/deep vein thrombosis (19%) and splanchnic vein thrombosis (15%). At the time of DOAC initiation, the median Charlson comorbidity index (CCI) was 7 (range 3-15); MELD score was 10 (range 6-24); and platelet count 150,000/ul (range 50,000-432,000). Thirty six (34%) patients had objectively diagnosed varices. Median follow up was 563 days (range: 7-2646). Bleeding requiring medical evaluation occurred in 32 (30.2%) patients. Major bleeding as defined by ISTH was experienced by 12 (11.3%) individuals. The most common source of bleeding was gastrointestinal tract (21.7%); other organs were less commonly affected (table 1). Hemorrhagic complication usually occurred early after starting anticoagulation (median 101 days; range 4-1356), and was the most common reason for discontinuation of anticoagulant treatment (14%), followed by completion of treatment (10%). On Cox proportional hazard modeling, rising BMI (HR: 1.032 per unit increase in BMI; p<0.05) and elevated bilirubin (HR: 1.223 per 1 mg/dL increase) were associated with increased risk of bleeding. Other clinical factors, including sex, type of anticoagulant used, platelet count, PT/INR, albumin, MELD score, varices, portal hypertension, concomitant aspirin use, and Charlson comorbidity index were not associated with bleeding risk. Thrombotic events while on DOAC affected 7 (6.7%) individuals, which included venous thrombosis in 4 (3.8%) and arterial thrombosis in 3 (2.9%) patients. No clinical factors were associated with increased risk of thrombosis. Conclusions: Our study is the largest series of patients with cirrhosis treated with DOACs. Bleeding complications with DOAC use in this population is high. Providers considering starting DOACs in patients with cirrhosis should consider the risk of bleeding in this population. Disclosures No relevant conflicts of interest to declare.