Despite the decrease in incidence of early clinical and subclinical rejection and increased 1-year graft survival in renal transplant patients, the rate of graft loss after the first year has been only moderately improved. Protocol biopsies obtained in the first year have shown rapid increase in the prevalence of IF/TA. This finding has been correlated with later allograft dysfunction and loss, mostly in cases of concomitant interstitial inflammation and fibrosis (1). The landmark study by Nankivell et al., performed in recipients of organs from deceased young donors under early cysclosporin-based immunosuppression, suggested two distinct phases of injury involved in IF/TA: an early tubulo-interstitial damage from ischemic injury and allograft rejection and, beyond 1 year, microvascular, glomerular and additional tubulo interstitial injury interpreted as secondary CsA toxicity (2). Since this publication, chronic antibody-mediated rejection has been better identified as leading causes of late graft dysfunction. Moreover, a recent study showed that most cases of kidney graft loss have an identifiable cause that is not idiopathic IF/TA or CNI toxicity and that alloimmunity remains the most common mechanism leading to failure (3). Thus, with the current immunosuppressive regimens and the input of molecular phenotyping, one may question the natural history of IF/TA.
©2011 The Authors Journal compilation©2011 The American Society of Transplantation and the American Society of Transplant Surgeons.