Delta Analysis of Posttransplantation Tubulointerstitial Damage

Abstract

CIF was a result of early ischemia-reperfusion injury, acute, subacute or persistent interstitial inflammation occurring in a time-dependent manner and was considerably modified by immunosuppressive therapy.

Are the current chronic allograft nephropathy grading systems sufficient to predict renal allograft survival?

“…These data confirmed the findings described by Nankivell et al (13) in which interstitial fibrosis showed an adverse impact on graft outcome (13)(14)(15)(16)(17). Furthermore, interstitial fibrosis is a common finding in other chronic kidney diseases besides chronic allograft nephropathy (13), having strong correlation with tubular atrophy and graft loss (13,18).…”

Transcriptional Profiling of Belatacept and Calcineurin Inhibitor Therapy in Renal Allograft Recipients

“…These increases in cv, ah, ci and ct correlated strongly with decreased cGFR at 36 months. This suggests that reduced tubulointerstitial and vascular damage seen in patients treated with belatacept is related to the better allograft function seen through 36 months (3,26,27), although multiple factors may contribute to CAI.…”

Renal Allograft Fibrosis: Biology and Therapeutic Targets

“…Thus, biopsies obtained from renal transplant recipients at day 0 and month 3 and 12 showed a rapid progression of IF scores from 19% to 27% at month 3 and 32% at month 12 (363). Other studies have also found that progression of IF is particularly prominent early after transplantation (365), suggesting that this is a window for therapeutic intervention. Additional analyses might further improve the predictive value of allograft biopsies such as the immunohistochemical detection of CD44 and vimentin (366), activation markers of parietal epithelial cells as markers of FSGS in the renal transplant (367), or immunohistochemistry aided analyses of peritubular capillaries to detect their early and progressive rarefaction in allografts (368).…”