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.
KeywordsRenal Transplantation Allograft Rejection Renal Allograft Rejection Episode Renal Allograft Recipient
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