Contrary to Persisting De-Novo DSA, Transient De-Novo DSAs After Lung Transplantation Do Not Constitute a Risk Factor for Patient and Graft Survival.

Approximately 50% of lung transplantation (LuTx) recipients develop de-novo DSA (dnDSAs) within the first year. In our institution, therapy is started only in case of clinical antibody-mediated rejection. The majority of dnDSAs disappears within 3-6 months; however, in some patients they persist. The aim of the study was to determine whether persistence of dnDSAs is associated with worse outcomes and as a consequence is worth of therapeutic intervention All patients, transplanted between 2010 and 2020. dnDSAs were defined as persistent if detectable for a time period longer than 6 months, otherwise were classified as transient. Four categories of mean fluorescence intensity were defined: I (1000-5000), II (5000-10000), III (10000-15000) and IV (>15000). 730 patients were included in the analysis, 153 patients (21%) developed dnDSAs. Eighty-one (11%) were transient while in 71 patients (10%) persisted for a period longer than six months. MFI categories were significantly different between transient and persistent dnDSAs (p<0.001): I (88% vs 17%), II (7% vs 33%), III (5% vs 19%), IV (0% vs 31%). 3 patients (4%) in the transient group and 26 (36%) in the persistent group developed clinical AMR (p<0.001) during the study period. Freedom from CLAD at 1-, 3- and 5-years was 93%, 86% and 63% in transient dnDSAs group compared to 85%, 49% and 34% in persistent dnDSAs group (p=0.001). Graft survival at 1-, 3- and 5-years was 90%, 78% and 68% in transient dnDSAs group compared to 81%, 59% and 45% in persistent dnDSAs group (p=0.008). Of not, the transient dnDSAs group showed similar 5-year survival as patients without dnDSAs (69% vs 74%, p=0.833). Contrarily, patients with persistent dnDSAs had low 5-year survival of only 48% (p=0.002). Persistent but not transient dnDSAs are associated with worse long-term outcomes. Further studies are needed to evaluate possible therapeutic strategies, aimed to prevent subclinical damage to the allograft. [ABSTRACT FROM AUTHOR]