Immunoglobulin Induction Therapy in Renal Transplant Recipients - Five Year Data of a Prospective Randomized Pilot Study.: Abstract# C1798

Intravenous immunoglobulin (IVIG) administration provides an established treatment modality to reverse steroid resistant rejection and to suppress alloantibody formation in sensitized recipients. To analyze graft protective effects of IVIG induction therapy, we performed a prospective randomized study in 50 renal transplant recipients who were randomly assigned to receive 7x10g IVIG and 7x10g iv albumin infusions, respectively. Immunological tests were performed up to 3 years, and clinical follow-up data were analyzed up to 5 years posttransplant. IVIG induction therapy did not affect sCD30 and sIL1-RA levels. However, regulatory autoantibody levels were increased in IVIG patients on day 10 (IgG anti-Fab and anti-F(ab)2: p≤0.005; IgA anti-Fab, anti-F(ab)2 and anti-hinge: p<0.05). IVIG patients showed an enhanced monocyte IL-10 production early posttransplant (day 30: p=0.011, unstimulated; p=0.049, LPS), followed by downregulated monocyte activation (p=0.024, 4-month neopterin) and profoundly suppressed 1-year CD4 helper activity compared to non-IVIG patients (p=0.003; logistic regression: p=0.001). However, between IVIG and non-IVIG patients no significant differences were found in 5-year patient and graft survival, graft function, incidence of acute rejections and chronic graft dysfunction. In non-IVIG patients, serum IgG and IgA levels were significantly decreased only within the first 20 days posttransplant compared to IVIG patients (p=0.001, IgG; p=0.039, IgA). The incidence of severe infectious disease, CMV viremia and CMV disease was not significantly different at any time point. Our data show that IVIG induction is associated with potentially graft protective immunological effects: increased regulatory autoantibody levels and upregulated monocyte IL-10 production early posttransplant, followed by downregulation of monocyte activation at 4 months and a profound decrease in CD4 helper activity at 1 year posttransplant. However, no improved clinical outcome (graft outcome; risk of infection) was found up to 5 years posttransplant in this cohort of immunologically low-risk patients. DISCLOSURES:Weimer, R.: Grant/Research Support, Astellas, Novartis.