Başkent Üniversitesi Yayınları

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Subject: search.filters.subject.Antibody-mediated rejection

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    Effective Therapy for Acute Antibody-Mediated Rejection With Mild Chronic Changes: Case Report and Review of the Literature
    (Başkent Üniversitesi, 2012-08) Osama Gheith,; Ibraheim, Mona; Saied, Tarek; Muzeirei, Ibraheem; Al-Waheeb, Salah; Nair, Prasad; Halim, Medhat; Nampoory, Narayanan; Al-Otaibi, Torki
    To reduce the long-term toxicities of immuno­suppressant drugs, corticosteroid-sparing and calcineurin-inhibitor–sparing immunosuppression protocols have become increasingly popular in managing kidney transplant recipients. The most vexing clinical condition caused by antibodies in organ transplants is antibody-mediated rejection. Limitations of the current antibody-mediated rejection therapies include (1) antibody-mediated rejection reversal tends to be gradual rather than prompt, (2) expense, (3) rejection reversal rates below 80%, (4) common appearance of chronic rejection after antibody-mediated rejection treatment, and (5) long-term persistence of donor specific antibodies after therapy. Because these limitations may be due to a lack of effects on mature plasma cells, the effects of bortezomib on mature plasma cells may represent a quantum advance in antihumoral therapy. Our experiences represent the first clinical use of bortezomib as an antihumoral agent in renal allograft recipients in Kuwait. We present 2 cases with resistant-acute antibody-mediated rejection to the standard therapies that were managed successfully with bortezomib.
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    Kidney Transplant in Highly Sensitized Patients After Desensitization With Plasmapheresis and Low-dose Intravenous Immunoglobulin
    (Başkent Üniversitesi, 2010-06) Yuan, Xiao-peng; He, Xiao-shun; Fu, Qian; Gao, Wei; Wang, Chang-xi
    Objectives: This study sought to evaluate the efficacy of plasmapheresis plus low-dose intravenous immunoglobulin in highly sensitized patients waiting for a deceased-donor renal transplant. Materials and Methods: Thirty-five highly sensitized patients (HLA class I panel reactive antibody > 50%) received plasmapheresis, plus low-dose intravenous immunoglobulin treatment. In 25 patients (group 1), a positive T- and/or B-cell cytotoxicity crossmatch was rendered negative by plasmapheresis, plus low-dose intravenous immunoglobulin treatment. Two patients did not receive renal transplants owing to persistent positive crossmatch. Eight patients already had a negative crossmatch before desensitization. During the same time, 32 highly sensitized patients (group 2), without de­sensitization, had a negative crossmatch and received deceased-donor renal transplants. Results: Group 1 showed a numerically higher rate of acute rejection (32.0% vs 21.9%; P = .6) and antibody-mediated rejection (20.0% vs 9.4%; P = .3), but the difference was not statistically significant. Four of 5 cases of antibody-mediated rejection in group 1 had a peak donor specific antibody titer ≥ 1:8. Comparable mean serum creatinine levels at 24 months were observed (group 1: 130 ± 38 µmol/L vs group 2: 123 ± 41 µmol/L; P = .5). No difference in Kaplan-Meier graft survival was found between group 1 and group 2 after follow-up of 52 ± 26 months (P = .7). Conclusions: Desensitization with plasmapheresis, plus low-dose intravenous immunoglobulin enables successful deceased-donor renal transplant in highly sensitized patients with a positive crossmatch. Antibody-mediated rejection occurred predominantly in recipients with donor-specific antibodies of high titers.
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    Donor-Specific HLA Alloantibodies: Long-Term Impact on Cardiac Allograft Vasculopathy and Mortality After Heart Transplant
    (Başkent Üniversitesi, 2008-09) Kaczmarek, Ingo; Ueberfuhr, Peter; Spannagl, Michael; Reichart, Bruno; Sodian, Ralf; Vicol, Calin; Schmoeckel, Michael; Beiras-Fernandez, Andres; Kauke, Teresa; Deutsch, Marcus-André
    Objectives: The clinical significance of anti-HLA-alloantibodies remains controversial. Recent studies have linked development of donor-specific HLA-antibodies to chronic allograft rejection and graft loss after heart, kidney, and lung transplants. We investigated the clinical impact of donor-specific humoral alloreactivity during the follow-up of heart transplant recipients. Patients and Methods: The sera of 213 heart transplant recipients were screened by enzyme-linked immunosorbent assay for HLA-antibody production. The antigen specificity of the detected HLA class I and class II antibodies was identified using a Luminex assay. Outcome variables were survival, cardiac allograft vasculopathy, and cellular rejection. Results: The cumulative incidence of alloantibody formation was 23/213 patients (10.8%). The majority of detected alloantibodies were donor-specific for HLA class II. Mean follow-up at antibody measurements was 7 ± 4.9 years. Freedom from vasculopathy at 5 and 10 years was 77.9% and 26% in donor-specific HLA-antibody-positive patients compared with 84.6% and 65.2% in antibody-negative controls (P = .025). Freedom from treated, biopsy-proven rejection was 44.4% for donor-specific HLA-antibody-positive patients compared with 70.2% in the controls (P = .06). Multivariate analyses identified donor-specific HLA antibody positivity as an independent risk factor for vasculopathy. Conclusions: Our results demonstrate a strong correlation between the development of donor-specific HLA antibodies and adverse outcomes after heart transplant. Detection of donor-specific HLA antibodies might identify high-risk patients and offer an opportunity for early clinical intervention and modification of immunosuppression.