Hippokratia 1998, 2(2):62-71
Rejection is the more frequent cause of renal allograft dysfunction. The diversity of clinical presentations of transplant rejection corresponds to a proportional diversity of histopathological lesions in the renal allograft. Moreover, renal graft may manifest changes which are the results of the immunosuppresive treatment. In addition, renal graft may be involved by all kinds of diseases occurring in the native kidney. Therefore, renal allograft insufficiency becomes a crucial question to both clinicians and pathologists. The latter is frequently asked to reveal the cause of graft dysfunction, from morphological changes, excluding or combining different etiologic mechanisms. Fibrin thrombi blocked capillaries and arterioles in hyperacute rejection, with a linear localization of IgM and C3 on the glomerular and intertubular capillary walls. The differential diagnosis comprises acute tubular necrosis, occlusion of the main vessels and ureteric obstruction. In acute rejection the allograft may show a wide spectrum of changes with varying degrees. Mononuclear cells, predominantly T-lump-hocytes infiltrate interstitium and tubules, provoked the characteristic change of tubulitis. Often, endothelitis, fibrin thrombi and foci of fibrinoid necrosis are present in the arterioles. The differential diagnosis comprise cyclosporine nephrotoxicity, CMV infection, acute tubular necrosis, acute bacterial or lymphocytic interstitial nephritis and posttransplant lymphoproliferative disorder. The characteristic lesions in chronic rejection are arterial narrowing and transplant glomerulopathy, associated with tubular atrophy and interstitial fibrosis. This review wants to use as a practical guide for histopathological appreciation of renal graft rejection; brief references to lesions due to causes other than immunologic incompatibility and discussion of differential diagnostic problems are added.