PubMed · 11099654
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D M Lublin. 2000. Universal RBCs.. https://doi.org/10.1046/j.1537-2995.2000.40111285.x
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BACKGROUND: In May 1997, a 19-year-old male patient of histo-blood group type O suffering from congenital end-stage heart failure accidentally received a cardiac allograft of type B and is still alive in fair condition. METHODS: In addition to conventional immunosuppressive therapy, plasma exchange (PEX), extracorporeal immunoabsorption (EIA), intravenous immunoglobulins (IVIG), and C1 inhibitor were used. RESULTS: Such treatment successfully reduced both IgM and IgG anti-B levels and complement hyperactivity and allowed to reach the state of accommodation without obvious signs of rejection. The patient has been surviving for 42 months; retransplantation with an O-type heart remained unnecessary. CONCLUSION: Humoral rejection has been avoided in this patient, with PEX, EIA, IVIG, and C1 inhibitor substantially contributing to this success. With future availability of such combined therapies, preferably before transplantation, vascular rejection events caused by preformed antibodies and complement (ABO mismatch or anti-HLA) could be prevented or treated.
BACKGROUND: Due to a severe shortage of suitable cadaveric allografts for children awaiting kidney transplants, we have performed a series of ABO-incompatible living kidney transplantations (LKT) at our institution. METHODS: Between July 1989 and March 2000, 16 pediatric patients (3 female, 13 male) underwent ABO-incompatible LKT. The mean age at transplantation was 10.9+/-4.3 years (range 5.1-15.0 years). The donor to recipient ABO blood antigen incompatibility was as follows: A1-->O, 5 patients; B-->O, 6 patients; A1B-->B, 2 patients; and A1B -->B, A1-->B, or B-->A1, 1 patient each. The median pretransplantation anti-A1 titers of eight A-incompatible recipients were 1:128 (IgM, range 1:16 to 1:512) and 1:32 (IgG, range 1:2 to 1:128). Median anti-B titers of seven B-incompatible recipients were 1:32 (IgM, range 1:4 to 1:128) and 1:8 (IgG, range 1:2 to 1:64). All patients received three or four sessions of plasmapheresis (PP) and/or immunoadsorption (IA) to remove the anti-A and/or anti-B antibodies before transplantation. Immunosuppression initially consisted of cyclosporine, methylprednisolone, cyclophosphamide, and antilymphocyte globulin. Splenectomy was performed on all recipients at the time of transplantation. RESULTS: The patients were followed for 6 to 122 months with a mean follow-up of 63 months. All 16 recipients who underwent ABO-incompatible LKT achieved a pretransplant isoagglutinin titer less than 1:8 with 3-4 sessions of PP/IA treatment. Of 16 patients, 10 patients had rebound increase in their IgM and/or IgG anti-A/B titers to greater than 1:64 or predepletion levels within 10 days posttransplantation. In addition, nine patients developed renal dysfunction in association with the rebound increase in their anti-A/B. One patient lost his graft because of uncontrolled delayed hyperacute rejection, whereas eight other recipients recovered completely with pulse steroids and PP/IA therapy. After the third week posttransplant, there was no correlation between the occurrence of AR and their isoagglutinin titers. Moreover, no antibody-mediated rejection was observed, even in recipients with continued high titer anti-A and/or anti-B antibodies. Patient survival is 100% to date. The actuarial 1-year and 5-year graft survival rates are 87% and 85%, respectively. No fatal infectious complications occurred despite the combination of splenectomy and immunosuppressive drugs. CONCLUSIONS: We have demonstrated that with adequate pre- and posttransplant management, successful kidney transplantation across the ABO barrier is possible in the pediatric population. "Accommodation" of the allografts occurred within 2 weeks of transplantation. Subsequently, the long-term graft outcome of ABO-incompatible LKT was comparable to that of ABO-compatible LKT.
BACKGROUND: Most investigations have revealed that the improvement in early graft survival has not resulted in a corresponding improvement in long-term graft survival. The risk factors for long-term graft survival should be clarified. METHODS: A single-center experience of 1100 consecutive renal transplant recipients who received kidneys from living donors from 1983 to 1998 was reviewed to clarify the time dependency of risk factors for long-term graft survival. We examined various possible risk factors, including HLA-AB and -DR mismatches, ABO-blood group incompatibility, graft weight, donor age and sex, recipient age and sex, and the presence or absence of acute rejection by using the time-dependent, nonproportional Cox's hazards model. RESULTS: Acute rejection episode, donor age, HLA-AB 4-antigen mismatches, ABO-incompatible transplantation, smaller kidney weight compared with the patient's body weight (Kw/Bw ratio less than 2.67), and transplantation from an unrelated living donor were risk factors for long-term graft outcome. Multivariate analysis for time-dependent risk factors showed that donor age of more than 60 years was the most important risk factor for long-term graft failure after 5 years posttransplantation (hazard ratio: 2.57). In contrast, acute rejection, ABO incompatibility, and nonrelated donors were significant risk factors for short-term graft failure within 5 years after kidney transplantation (hazard ratios: 2.68, 1.57, and 1.69, respectively). CONCLUSIONS: Donor age of more than 60 years was a crucial risk factor affecting long-term graft survival. In contrast, acute rejection, ABO incompatibility, and nonrelated donors were significant risk factors for short-term graft failure.