ABSTRACT
During the 1980s and early 1990s there was clearly a failure to un derstand the phenomenon then called “chronic rejection”. The Banff meeting of pathologists coined the term “chronic allograft nephropathy” and by doing so disconnected the appearance of chronic graft damage from any presumption of it being solely due to an immune pathophysi ological mechanism. In common parlance CAN has become litde more than short hand for progressive loss of kidney function through graft fibrosis, leading to graft failure and the need for dialysis. New think ing amongst the histopathologists has now lead to abandonment of Chronic Allograft Nephropathy and replacement with “IFTA” or interstitial fibrosis and tubular atrophy. This has been designed to be taken simply as a pathological description of the appearance of the kidney biopsy.4 It will not be the rallying cry that “CAN” has been, but one can understand the reason for change because “CAN” has taken on a life of its own, disconnected from underlying clinical realities and
permitting abrogation of responsibility for prevention and treatment in the individual patient. Over the past few years longitudinal histological studies have helped in the understanding of the limited responses to injury that the kidney possesses leading to development of strategies for both prevention and treatment.
