These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Pretreatment of renal allograft recipients with immunosuppression and donor-specific blood.
    Author: Anderson CB, Tyler JD, Sicard GA, Anderman CK, Rodey GE, Etheredge EE.
    Journal: Transplantation; 1984 Dec; 38(6):664-8. PubMed ID: 6239414.
    Abstract:
    The induction of immunologic unresponsiveness to improve renal allograft survival was attempted in 64 patients by the pretransplant administration of donor-specific whole blood or buffy coat in conjunction with continuous azathioprine immunosuppression. All donor/recipient combinations were at least one-haplotype-disparate. Presensitization, defined as a positive Amos or antiglobulin crossmatch or a high-titer (greater than 1:8) B-cell-positive crossmatch, was present in 6 patients and not present in 58 patients. Attempts at desensitization of the already sensitized group were uniformly unsuccessful. Treatment of the 58 nonpresensitized patients resulted in transient sensitization in 2 patients, permanent sensitization in 1 patient, and no evidence of sensitization in 55 patients. Fifty-three patients underwent renal transplantation from the specific blood donor, and only two have experienced renal allograft rejection loss during a mean follow-up period of 22 months (5-45 months); 57% have never experienced a rejection episode. The two-year renal allograft survival rate was 85%. This is significantly (P less than 0.01) better than our historical experience of 64% with one-haplotype living-related transplants. The low rate of sensitization (5%) has permitted almost all patients to undergo eventual renal transplantation from the specific blood donor. This and the low rate of rejection (4%) argues for a modification of the immunologic response, rather than a selecting-out process as the mechanism for improved allograft survival.
    [Abstract] [Full Text] [Related] [New Search]