At autopsy, all anastomoses of both allografts were intact. The loops of small bowel were densely adherent to one another and to the peritoneal wall. The liver was fibrotic and cholestatic, consistent with damage due to hyperalimentation. The heart was ecchymotic and had hemorrhagic cavities in both ventricular walls which proved to be abscesses caused by Aspergillus fumigatus; there was extensive fungal infection, with involvement of the allograft kidney, native kidneys, lungs, and allograft bowel. In the serosa and, to a lesser extent, the mucosa of the allograft bowel were extensive infiltrates of Epstein-Barr virus associated polymorphous PTLD. No specific evidence of rejection of either allograft was found at autopsy.
The nature of the original kidney disease is unclear. The native kidneys had multiple sclerotic glomeruli, but intact glomeruli do not exhibit specific features of glomerulonephritis. The glomerulosclerosis is predominantly cortical, a pattern different from the juxtamedullary involvement seen in focal segmental glomerulosclerosis. Many fetal glomeruli, of unknown significance, are present. There is mild tubulointerstitial nephritis and fibrosis, which may have resulted from antibiotic therapy, but the degree of damage seems insufficient to account for renal failure.