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E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
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Abstract titles should be brief and reflect the content of the abstract.
Plasma cell-rich acute rejection is a quiet less common type of allograft rejection in renal transplantation. The characteristic graft biopsy finding is the presence of more than 10% inflammatory cells being mature plasma cells. The attributable causes are infection and poor immune-suppression. With unknown pathogenesis and not well defined treatment; patient's survival is poor.
A renal transplant recipient with dialysis vintage of 4 months, donor being the sister ,ABO compatible, induction by anti-thymocyte globulin, on triple immunosuppression with transplant done one and a half year back presented to outpatient department with slowly rising creatinine from 0.8 to 1.8 in last past 5 months. Patient got her tacrolimus serum levels monitored on regular basis which were satisfactory. At the same time she was investigated for CMV viremia and BK-viremia. Both of which were negative. She was non oliguric and non-uremic. The basic renal disease was unknown and the urine didn’t had active sediments. In a fix the nephrologist underwent a graft biopsy.
The biopsy was suggestive of plasma cell-rich acute rejection with acute T-cell mediated rejection grade 1B: Interstitial inflammation involving >25% of non-sclerotic cortical parenchyma(i3) with severe tubulitis (t3) involving 1 or more tubules in a background of chronic active TCMR grade1B:Interstitial inflammation involving >25% of sclerotic cortical parenchyma(i-IFTA3) and >25% of total cortical parenchyma (ti3) with severe tubulitis (t3 and t-IFTA3).Stain for C4d negative in peritubular capillaries. Stain for SV40 was also negative. Banff scores :i3;t3;v0;g1;ptc1;C4d0;ci3;ct3cv0;cg0;ptcml-NA;ti3;i-IFTA-3,pvl0 (Banff 2019- update).Patient’s biopsy had component of TCMR , peri-tubular capillaritis and glomerulitis as well however C4D was negative. Treatment was started from 27.8.25 .Patient received intravenous methylprednisolone (500 mg/kg for 3 days) , anti-thymocyte globulin (1.5 mg/kg/day for 4 days) and 1 cycle of bortezomib (1.3 mg/m2 on days 1, 4, 8, and 11).Following the treatment her creatinine started coming down within 2 weeks to 1.4
Plasma cell rich acute rejection is classically taken as acute cell mediated rejection but very often there are features of acute antibody mediated rejection as well. Anti-thymocyte globulin used in this case was directed towards the TCMR whereas bortezomib was directed towards the plasma cells .This drug induces plasma cell apoptosis and has been successfully used to decrease alloantibody levels and treat concurrent antibody and cell-mediated rejection processes. To date, there is no gold standard for efficient treatment of PCAR. Reports suggest use of methyl prednisolone (500 mg/kg), 7 sessions of plasmapheresis, anti-thymocyte globulin (3–5 mg/kg/day for 10 days), rituximab (2 doses at 375 mg/m2), and bortezomib (1 cycle at 1.3 mg/m2), with 2-year graft survival rate after rejection of 90%.
