COLD-REACTIVE ALLOANTIBODIES AND ALLOGRAFT MALFUNCTION OCCURRING IMMEDIATELY POSTTRANSPLANT

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Abstract
Certain kidney allografts function promptly, whereas others subjected to similarly optimal procurement and preservation methods do not. Such unexplained allograft malfunction (AM) could be due to the presence of cold-reactive IgM alloantibodies (i.e., lymphocytotoxins and agglutinins) present in renal transplant recipients. Investigations were undertaken to determine whether the presence of such alloantibodies was associated with any histological abnormalities. Pretransplant and 1-h posttransplant biopsies were analyzed from 49 cadaveric renal allografts that came from ideal donors and were subjected to optimal preservaiton. No correlation could be made between AM and the severity of renal tubular cell disruption. Glomerular lesions in the posttransplant biopsy correlated significantly with the development of AM. Segmental glomerular intracapillary red blood cell aggregates and fibrin deposition were present in 71% of biopsies in the 21 allografts with AM, whereas such lesions were present in 29% of biopsies in the 28 allografts with immediate function (P < 0.005). Development of glomerular lesions correlated significantly with the presence of cold-reactive lymphocytotoxins (CRL) in the recipient (60% vs. 9%). Sea containing CRL also had IgM antiendothelial cell antibody. Another possible mechanism for lack of prompt allograft function is a self-limiting vascular injury, that occurs in the cold and is immune-mediated.

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