Localization of fluorescein‐conjugated heat‐aggregated IgG (FA IgG) was demonstrated by immunofluorescence in renal glomeruli of 16 of 69 patients with glomerulonephritis. FA IgG bound more frequently in kidney biopsies from patients with diffuse glomerulonephritis and depressed renal function, and localized selectively in glomeruli that contained heavy deposits of IgM, C3, and C4. The factors that caused FA IgG to bind were specifically reactive with the Fc piece of the IgG molecule and were resistant to 56°C heat for 30 minutes. Localization of FA IgG in the kidney did not correlate with the presence of soluble immune complexes or detectable antiglobulin antibodies in the sera. Binding of FA IgG was also seen in glomeruli and arteries of 18 of 21 kidney allografts studied at the time of impending rejection. But the factors responsible for binding FA IgG in the allografts were heat labile and thus could have been Clq. Although the role of these “antiglobulins” in the immunobiology of glomerulonephritis remains unknown, the fact that they occurred mainly in patients with relatively severe glomerular injury suggests that they could play some part in promoting renal glomerular injury.

Direct immunofluorescence studies of 14 human cardiac allografts revealed extensive deposits of immunoglobulin in the sarcolemma, muscle fibers, and in successive layers within the thickened intima of the coronary arteries. In contrast, original hearts from eight recipients and biopsies of six donor hearts taken before transplantation showed little bound immunoglobulin. Sarcolemma-bound IgG was seen significantly more frequently in hearts which succumbed to early rejection. Sera collected before transplantation from 15 to 17 cardiac allograft recipients contained antibodies reactive with cardiac muscle from unrelated donors by indirect immunofluorescence, but not with kidney tissue or skeletal muscle from the same unrelated donors. Pretransplant sera from eight of nine patients also contained antibodies which reacted with the patient's own heart. These results suggest that human cardiac allografts provoke a strong humoral as well as a cell-mediated rejection response and provide evidence which links deposition of immunoglobulin within the arterial intima to the evolution of the obliterative vascular lesion seen in the majority of the cardiac allografts.