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Extracorporeal membrane oxygen (ECMO) is increasingly used as a bridge to lung transplantation. Although other mechanical circulatory support devices have been associated with a transfusion-independent increase in calculated panel reactive antibodies (CPRA), it is unknown whether ECMO is a sensitizing exposure. In this single center retrospective cohort study of lung transplant candidates between 5/1/2015-6/30/2021, antibodies against human leukocyte antigens (HLA-Ab) were evaluated at the time of ECMO initiation and weekly thereafter. Multivariate logistic regression was used to evaluate associations between CPRA increase and ECMO exposure adjusting for a history of any packed red blood cell (PRBC) transfusion and female gender. Sixty-two candidates were placed on ECMO as a bridge to transplant. Of these, 39 (62.9%) either had available HLA-Ab screens from pre- and post-ECMO initiation or multiple HLA-Ab screens post-ECMO. Of the 250 non-ECMO exposed recipients, 224 (89.6%) had multiple pre-transplant screens and served as the comparison cohort. Nine (23.1%) ECMO bridged recipients had an increase in CPRA, compared to 16 (7.1%) of non-ECMO exposed recipients (Fisher's exact p=0.005). Among those with increased CPRA, the median increase was 6% in ECMO bridge patients and 9% in non-ECMO exposed patients. After adjusting for covariates, however, ECMO bridge was not an independent risk factor for increased CPRA (OR=1.85, 95% CI 0.58-5.95, p=0.30). A history of PRBC transfusion trended toward an association with increased CPRA (OR=2.93, 95% CI 0.98-8.78, p=0.06). Pre-lung transplant ECMO was not independently associated with an increase in CPRA when adjusting for PRBC transfusion, although the study was underpowered for small or moderate effect sizes. Where clinically appropriate, PRBC transfusions should be limited in these patients. [ABSTRACT FROM AUTHOR]

Pre-transplant antiphospholipid antibodies (aPLab), including anticardiolipin (aCL) and anti-B2 glycoprotein-I (aB2GPI), may be associated with thrombotic complications and graft loss in kidney and liver transplant recipients. The objective of this study was to evaluate the prevalence and impact of aPLab on post-operative thrombotic and bleeding complications in lung transplant recipients. This was a single center retrospective cohort study of patients who were evaluated and transplanted between 1/1/2018-11/30/20. All candidates were screened for aPLab. We compared post-operative arterial and venous thrombotic events, treated as a combined endpoint, in recipients with and without aPLab (Fisher's exact test). Among recipients with aPLab, we recorded major bleeding events—defined as requiring blood transfusion or surgical exploration—while on therapeutic or prophylactic dose anticoagulation (AC). There were 100 patients who were evaluated and transplanted during the study period, 19 (19.0%) of whom had aPLab (Figure 1). Among these, 7 (36.8%) had pre-transplant deep vein thrombosis (DVT) or arterial thrombotic events. After transplant, 7 (36.8%) had new symptomatic DVT or arterial thromboses compared to 20 (24.7%) recipients without aPLab (p=0.39). Ten patients with aPLab were fully anticoagulated post-transplant, either because of prior or new thrombotic events. Of these, 6 (60.0%) had major bleeding. One aPLab patient had major bleeding on prophylactic AC. The majority (85.7%) of patients with major bleeding were on renal replacement therapy or had an eGFR <30. The one-year survival rate among recipients with aPLab was 89.5%. The presence of a pre-transplant aPLab was not associated with an increase in new symptomatic DVT or arterial thrombotic events following lung transplant although the study was underpowered for small or moderate effects. The decision to anticoagulate patients with aPLab should account for other risk factors for bleeding including renal insufficiency. [ABSTRACT FROM AUTHOR]