| Abstract: | Second-set kidney transplant reactions occur in decomplemented dogs. The microscopic features of the reaction under such conditions indicate that the typical acute inflammatory reaction has occurred. Since the factors (presumably antibodies) mediating the second-set reaction are not dependent on complement fixation it is unlikely that HL-A antibodies, which are dependent on complement fixation for cytotoxicity, can be implicated in so-called hyperacute rejection (i.e. second-set rejection) in humans. The microscopic features of a genuine second-set reaction in humans are identical to those originally described in the dog. Since the first observable sign of the second-set kidney reaction is vasoconstriction of the outer cortical vessels, it is essential to establish how a severe antigen-antibody reaction can evoke such a rapid destruction of a kidney allotransplanted to a previously sensitized recipient. It is glomerular basement membrane which first bears the brunt of the second-set reaction. Tubular damage appears to follow gross ischaemia resulting from afferent renal vasoconstriction. Since the antigens of renal basement membrane are not represented on the lymphocytes, serious problems arise in attempting to assess renal histocompatibility by lymphocyte markers. |
