Arterial endothelialitis in chronic renal allograft rejection: a histopathological and immunocytochemical study.
Transplantation is the preferred method of renal replacement therapy in end-stage renal failure. Short- and medium-term graft survival is good but, in the longer term, grafts are lost due to vascular obliteration, i.e. chronic vascular rejection. The pathogenesis of these changes is unclear. We carried out a histopathological and immunocytochemical study of 31 vessels from 20 graft nephrectomies. Four patterns of arterial pathology were identified: (1) subendothelial inflammation ('endothelialitis') with little intimal thickening; (2) 'Endothelialitis' with thickening; (3) Intimal thickening without 'endothelialitis'; and (4) Intimal thickening with calcification and cholesterol clefts ('natural atherosclerosis'). We suggest that the lesions of chronic vascular rejection evolve, at varying rates, from an early 'endothelialitis' to a later stage with pronounced intimal thickening but no subendothelial inflammation. These changes probably reflect a delayed type hypersensitivity response involving activated macrophages and T lymphocytes and smooth muscle cell proliferation.
Gouldesbrough
D R
DR
Department of Pathology, University of Edinburgh Medical School, UK.
Axelsen
R A
RA
D000293:Adolescent; D000328:Adult; D000368:Aged; D001158:Arteries / Q000473:pathology*; D004730:Endothelium, Vascular / Q000473:pathology*; D005260:Female; D006084:Graft Rejection; D000949:Histocompatibility Antigens Class II / Q000032:analysis; D006801:Humans; D007150:Immunohistochemistry; D007249:Inflammation / Q000473:pathology; D016030:Kidney Transplantation / Q000276:immunology*; D008297:Male; D008875:Middle Aged; D009687:Nuclear Proteins / Q000032:analysis; D018809:Proliferating Cell Nuclear Antigen
D000949:Histocompatibility Antigens Class II; D009687:Nuclear Proteins; D018809:Proliferating Cell Nuclear Antigen