PURPOSE OF REVIEW: Chronic allograft nephropathy has fallen into disfavor as a morphologic term to describe parenchymal scarring in the renal allograft, with a recommendation that this be replaced by the more descriptive term 'interstitial fibrosis and tubular atrophy'. However, neither term addresses the underlying cause of the scarring. This review focuses on whether all interstitial fibrosis and tubular atrophy in the renal allograft has the same implications for long-term graft survival, and whether there are specific features of interstitial fibrosis and tubular atrophy that can be used to identify its underlying cause.
RECENT FINDINGS: Results from a number of studies indicate that interstitial fibrosis and tubular atrophy, when associated with interstitial inflammation, is a strong predictor of graft loss, much more so than interstitial fibrosis and tubular atrophy alone. Most notably, findings from the multicenter Long-Term Deterioration of Kidney Allograft Function study, designed to identify the causes of late allograft dysfunction, showed interstitial inflammation in the areas of interstitial fibrosis and tubular atrophy (i-IF/TA) was predictive of reduced time to graft failure, even after adjustment for serum creatinine. In addition, the presence of i-IF/TA correlates with increased acute kidney injury gene transcripts. However, neither interstitial fibrosis and tubular atrophy nor i-IF/TA is associated with any specific cause of chronic graft injury.
SUMMARY: Although (i-IF/TA), especially when widespread, is clearly associated with reduced renal allograft survival and molecular markers of active graft injury and repair, there is presently no reliable way, using either morphology alone, immunohistochemistry, or molecular techniques, to differentiate i-IF/TA (or interstitial fibrosis and tubular atrophy alone) resulting from different causes.
Mendeley saves you time finding and organizing research
Choose a citation style from the tabs below