*Purpose: In contrast to recurrent immune complex-mediated glomerulonephritis (ICGN), de novo ICGN of the allograft is poorly characterized. We hypothesize that alloimmunity results in immune-complex deposition (ICD) manifesting as de novo ICGN in the allograft.

*Methods: Using the Columbia University Medical Center pathology database, we performed a retrospective review of allograft biopsies between 01/01/2011 and 12/31/2017. Clinical and laboratory data, native biopsies and allograft biopsies were reviewed allowing us to identify 35 cases of definite de novo ICGN and 65 cases of definite recurrent ICGN. All patients underwent testing for class I and II donor-specific HLA antibodies (DSA) by Luminex ^®SA at the time of kidney transplant (KT) and/or at the time of ICGN discovery.

*Results: A broad range of immune complex-mediated injuries was observed. Table 1 compares the demographic and clinical data of both groups. Both groups had a similar prevalence of positive DSA at the time of KT (de novo ICGN:12.9%, recurrent GN:8.8%, p=0.49). However, up to 36.7% of patients with de novo ICGN as compared to only 18.2% of patients with recurrent ICGN (p=0.04) had positive DSA at the time of ICGN discovery (Figure 1). There were no differences between groups in graft failure rates, time to graft failure or last creatinine on follow up (Table 1).

*Conclusions: DSA to donor HLA antigens are associated with ICD which can be interpreted as de novo ICGN on pathology. The significance of these deposits and their relationship to alloimmunity and allograft antibody-mediated rejection deserves further investigation.

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