Clinical Histocompatibility Testing in Renal Transplantation
Allograft rejection is due to recipient sensitization to foreign, donor histocompatibility antigens resulting in activation of multiple immunological vectors of tissue destruction (Medawar, 1944; Stiller and Sinclair, 1979; Carpenter and Morris, 1979). Due to the functional reserve of the kidney, signs of rejection are frequently evident only after extensive damage to the allografted tissue. The clinical diagnosis of renal-allograft rejection is based on patient symptoms and signs, namely, fever, weight gain, swelling, pain, or hypertension. Laboratory evidences of reduced renal function include elevated serum creatinine and blood urea nitrogen, decreased creatinine clearance, increased albumin clearance, and lymphocyturia. Tissue typing and cross-matching procedures attempt to minimize the tissue incompatibility and avert grafting into presensitized hosts. Since the signs, symptoms, and laboratory evidences of rejection are late events, immunological evidences of recipient activation of a primary immune response may alert the clinician, thereby affording the possibility for prompt initiation of immunosuppressive therapy to minimize the extent of tissue damage. However, due to the variety of antibody and cell-mediated components of immune mechanisms documented in rejection (Busch et al., 1976, 1977) recipient immune activation cannot always be documented. Indeed, there is no known test that is immunologically specific, sensitive, predictive, or at least confirmatory, and associated with few false-positive reactions.
KeywordsRadionuclide Flare Glutamine Triad Thymidine
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- Buda, J., Jacob, G., Lattes, C., Stevens, L., Sotelo, J., Suciu-Foca, N., Weil, R., and Reemstma, K., 1975, Prediction of humoral rejection in renal allograft recipients by MLC inhibition, Transplant. Proc. 7:671.Google Scholar
- Collaborative report of the Scanditransplant, 1975, Lancet 1:240.Google Scholar
- Descamps, B., Gagnon, R., Debray-Sachs, M., Barbanel, C., and Crosnier, J., 1975, Lymphocyte-dependent and complement-dependent antibodies in human renal allograft recipients, Transplant. Proc. 7:635.Google Scholar
- Kerman, R., and Stefani, S., 1976, Immunological evaluation of patients with solid tumors before and after radiotherapy, in: Neoplasms Immunity: Mechanisms (R.G. Crispen, ed.), pp. 109–120, University of Illinois Press, Chicago.Google Scholar
- Kerman, R.H., Roesler, H., and Kahan, B.D., 1978, Specific stimulation of active T-rosette forming cells by 3M KC1 solubilized antigen, Fed. Proc. Fed. Am. Soc. Exp. Biol. 37:1686.Google Scholar
- Kissmeyer-Nielson, F., Olsen, S., Peterson, V., and Fjeldborg, O., 1966, Hyperacute rejection of kidney allografts associated with pre-existing antibodies against donor cells, Lancet 2:663.Google Scholar
- Medawar, P.B., 1944, The behavior and fate of skin autografts and skin homografts in rabbits, J. Anat. (London) 78:176.Google Scholar
- Rashid, A., Sengar, D.P.S., and Harris, T.E., 1975, Role of mixed-leucocyte-culture blocking factor activity in human kidney transplants, Transplant. Proc. 7:667.Google Scholar
- Soulillon, J.P., Mouton, A. de, Reyrat, M.A., and Guenell, J., 1979, Role of anti-donor B lymphocyte antibodies in definitive allograft rejection, Transplant. Proc. 11:770.Google Scholar