Lung Transplantation: DSA to AMR Trajectory

185 subjects had positive HLA DSA (54.73%) detected at a median of 33 days post-transplantation. (IQR 9.0-236.8) DSA was predominantly de novo (n=119, 64.3%) than preformed (n=66, 35.7%), class II than Class I (76.44% vs. 20.24%, p<0.01). Of 185 DSA+ patients, 92 developed clinical AMR, 27 no AMR, and 66 had insufficient data to adjudicate clinical AMR. AMR developed at a medium of 130 days from DSA detection. (IQR 58- 504) The prevalence of clinical AMR was 23.65%(N=92): definite (N=6, 6.5%), probable (N=16, 17.4%) and possible (N=70, 76%).De novo DSA showed a higher rate of progression to AMR than preformed DSA (62.5% vs. 32.5%, p<0.01). %ddcfDNA levels correlated with AMR risk: median %ddcfDNA for de novo DSA that lead to AMR was 2X higher than de novo DSA that did not lead to AMR (1.55 vs. 0.88 p=0.016). Preformed DSA that lead to AMR had a median %ddcfDNA of 1.47 versus 0.87 in the preformed DSA that did not lead to AMR (p=0.014). DSA that did not lead to AMR showed higher %ddcfDNA levels than DSA negative, non-rejection timepoints. (0.87 vs. 0.33, p<0.01) CONCLUSION: De novo and preformed DSA showed greater allograft injury than non-rejection DSA- timepoints. De novo DSA progresses to AMR at a higher rate than preformed DSA. Preformed or de novo DSA that progresses to AMR causes more lung injury than DSA with no AMR. %ddcfDNA could be used to identify and treat high-risk DSA.