PATHOLOGICAL CHANGES IN 37 HUMAN RENAL HOMOTRANSPLANTS TREATED WITH IMMUNOSUPPRESSIVE DRUGS
Authors: Porter K. A. , Marchioro T. L. , Starzl T. E. 
Published: December 2008

Pathological changes in thirty‐seven human renal homotransplants are described. All the patients had been treated with Imuran, prednisone and actinomycin C; ten had also received local X‐irradiation to the transplant.

Fifteen of the transplants were from patients in a rejection phase. Most of these kidneys were enlarged because of interstitial oedema and several were speckled with petechial hemorrhages. There was fibrinoid necrosis of afferent arterioles and interlobular arteries in twelve of the transplants, and the peritubular capillaries were disrupted in ten. Swelling of the arteriolar endothelial cells, fibrino‐platelet and fibrous intimal thickening of interlobular arteries were also common. In most of the transplants there was a light infiltration with small lymphocytes, plasma cells and a few larger pyroninophilic cells. Similar changes were present in the pelvis and ureter.

Twelve of the transplants came from patients whose last rejection episode had been clinically reversed 14 to 117 days previously. AH these kidneys were enlarged because of compensatory hypertrophy. Seven showed some intimal thickening of the interlobular arteries and in three there was fibrinoid necrosis of arteriolar walls. Tubular atrophy, interstitial fibrosis and a light cellular infiltration were also common changes. Only one kidney appeared normal.

Three transplants came from patients who had not experienced clinical evidence of a rejection episode. One showed acute tubular necrosis due to prolonged ischemia at the time of transplantation; one was almost normal; the third showed vascular lesions suggestive of old unrecognised rejection.

Seven transplants had either not functioned or developed some complication necessitating their early removal. One of these was infarcted due to obstruction of the venous drainage; two showed massive acute tubular necrosis due to ischaemia; two, which were incompatible with their hosts on the basis of ABO blood groups, failed to excrete urine and showed distension of the arterioles and glomerular capillaries with erythrocytes; one bled uncontrollably from the pelvis; one came from a patient who died at twelve hours from hyperkalemia and hyponatremia during a massive post‐operative diuresis.

This work was aided by grants A‐6283, A‐6344, HE‐07735, AM‐07772, AI‐01452, and OG‐27 from the U.S. Public Health Service, and by a grant from the Medical Research Council.

The necropsies on cases described in this paper were either performed or supervised by Drs Coral Cotterall, Doris Courington, Carol Ewing, R. B. Hill, J. Jamroz, D. W. King, D. M. Lang, Martha La Via, Elizabeth Macintyre, N. McGrath, J. C. Maisel, C. G. Massion, D. R. Meekin, H. B. Neustein, S. Ryan, and D. E. Smith. We would like to thank all these pathologists for making this study possible. We are particularly grateful to Dr D. T. Rowlands, who supervised some of the necropsies, for his helpful co‐operation throughout this study.

Expert assistance in preparing the sections and photomicrographs was given by Miss Jane Rendall.