Accelerated arteriosclerosis: a form of transplant arteriopathy

Abstract

Purpose of review: Terminology for posttransplant renal arterial lesions is confusing, with multiple terms being applied, the more common among them being the comprehensive terms, transplant arteriosclerosis and transplant atherosclerosis; endarteritis, for intimal lesions with an inflammatory component; and finally for advanced lesions with or without intimal inflammation, transplant arteriopathy. However, these latter lesions may present the appearance of banal arteriosclerosis, albeit more advanced expected on the basis of donor age. This review explores the distinctions to be drawn among these various descriptive terms.

Recent findings: Cell-mediated arterial lesions due to T-cell cell-endothelial interactions and antibody-mediated lesions, due to antiendothelial cell antibodies, show many common features: myofibroblasts, some of recipient origin, laying down extracellular matrix. However, they differ in that cell-mediated intimal lesions initially have a prominent leukocytic component, usually absent in antibody-mediated lesions. The antibodies most frequently implicated are antihuman leukocyte antigen class I and class 2 antibodies. With the exception of a sometimes more cellular intima and initial absence of dense collagen and elastic fibers, these latter lesions resemble those of arteriosclerosis of aging.

Summary: Many instances of lesions designated as transplant arteriopathy are morphologically similar or identical to typical renal arteriosclerosis and could equally be regarded as accelerated arteriosclerosis.