The nature of experimental second-set kidney transplant rejection. 6. The ultrastructural features: an immunological dilemma.

Recipients which have already rejected allografts of skin react rapidly and violently against a subsequently allotransplanted kidney. This is the renal allotransplant second-set reaction, the primary manifestation of which is a sudden severe afferent vasoconstriction. As a result of this vasomotor disturbance, red blood cells and platelets sometimes aggregate in the glomerular capillaries and the renal tubule cells suffer necrosis. The precipitating cause of the vasomotor disturbance has not been determined but platelet aggregation can be ruled out since in ancrod (Arvin)-treated recipients this does not occur although a second-set reaction develops. No evidence of glomerular basement membrane damage, due either to anti-glomerular basement membrane antibodies or antigen antibody complexes, was detected by the current ultrastructural studies. Since in these experiments the recipients were previously sensitized by skin allografts, a cytotoxic factor which is directed against specific renal components should not be expected to mediate the renal allotransplant second-set reaction. There is, at some structural level, common antigenicity between skin, heart and kidney and, since all three tissues succumb to changes in their vascular systems, it suggests some common antigenic factor in blood vessels. The features of the renal second-set reaction have been compared with other established renal immune disease states but none can compare in rapidity and severity of action with the second-set reaction.