*Purpose: Liver allografts are resistant to antibody mediated rejection (AMR) in the presence of preformed alloantibodies. In most cases donor specific antibodies (DSAs) disappear a few months after liver transplantation (LTx). Increasing reports highlight a potential deleterious role of preformed DSAs in LTx survival. There is a little knowledge on impact of induction immunosuppression (IS) on preexisting or denovo development of DSAs in LTx.

*Methods: We conducted a retrospective single center review of prospectively collected data on 50 ABO compatible LTx from 2016 to 2018. Our induction regimen is solumedrol 500mg before reperfusion, 250 mg on post-operative day 1, 125 mg on day 2, and then taper to steroid free at 6 months. Maintenance IS consists of mycophenolate 1000 mg/day and tacrolimus with trough levels 6-8 ng/mL. Patients (pts) are monitored for development of DSAs. Continuous variables are reported as mean with standard deviation, analyzed using unpaired t test. For categorical variables Fisher’s test was used, P of <0.05 was considered significant.

*Results: Pts mean age at LTx was 36.9 years, predominantly Caucasians (78%). Etiology of liver disease was: HCV infection 42%, Alcohol 36%. The mean follow up was 407 ±270 days. Mean PRA was 24%, 2 patients had positive T/B cell CXM, 1 patient had positive B cell CXM due to presence of DSAs. Three pts had Class II DSAs only, 2 pts had CI & CII antibodies and 2 pts had CI antibodies at the time of LTx. 10 pts developed biopsy proven ACR within first 12 months and were treated with pulse dose steroids. One patient developed AMR 20 days post-LTx. Treatment consisted of apheresis, IVIG and Bortezomib. One year graft & patient survival were 96%. Class I & II DSAs MFI at the time of LTx were 53195 ± 44999, & 22292 ± 27717 respectively. At last follow up, 18% of patients developed denovo DSAs [7 CII only, 3493 ± 2946 MFI, one CI 4531 MFI and CII ± 1954] MFI. Two pts with pre-existing CI & II DSAs cleared only CI antibodies. There was a significant drop in cumulative CI+CII and CI DSAs from transplant to last follow up with P = 0.05 and 0.02 respectively. In the rejection group, 4 out of 11 pts were noted to have DSAs. There was no significant difference in DSAs MFIs in pts with & without rejection, P= 0.72. There was no significant difference in AST, ALT, INR, albumin, and total bilirubin levels in pts with & without DSAs.

*Conclusions: Steroid induction alone appears to be sufficient in controlling DSAs as evident by drop in pre-existing antibodies strength. LTx pts may still develop denovo or may not be able to clear CII DSAs. More prospective studies are required to determine if choice of induction therapy will have an impact on CII antibodies dynamics.

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