It appears that in human renal isografts glomerulonephritis in the transplant may be a recurrence of the original disease. In the allograft, nephritis may be either recurrence, an intrinsic part of the rejection process itself, or acquisition de novo of the disease. A number of parallels to both antiglomerular basement membrane disease and circulating antigen-antibody complex disease in the animal model are suggested, but with the possible exception of an occasional demonstration of anti-GBM disease, proof that such mechanisms operate in the glomerulonephritis developing in the human allograft is at present lacking.