2008
DOI: 10.2215/cjn.03040707
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Late Kidney Allograft Loss

Abstract: Despite dramatic improvements in immunosuppression, late graft loss after kidney transplantation remains a common and difficult problem. Histologic evaluation may reveal changes related to BK polyomavirus infection, hypertension, or calcineurin inhibitor toxicity, which can help to guide therapy. The designation chronic allograft nephropathy should thus be reserved for biopsies with tubular atrophy and interstitial fibrosis without an apparent cause. Although the cause clearly includes both antigen-dependent a… Show more

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Cited by 103 publications
(76 citation statements)
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“…[30][31][32] Taking into account the role of calcineurin inhibitors in the progression of chronic allograft nephropathy and their importance in mediating the epithelial to mesenchymal transition, one can speculate that the nephroprotective effects of epoetin-b may be at least partly caused by the inhibition of calcineurin inhibitor-induced epithelial to mesenchymal transition by RHuEPO. Thus, correcting tissue hypoxia by raising Hb levels adds to the tissue protective effects of RHuEPO.…”
Section: Discussionmentioning
confidence: 99%
“…[30][31][32] Taking into account the role of calcineurin inhibitors in the progression of chronic allograft nephropathy and their importance in mediating the epithelial to mesenchymal transition, one can speculate that the nephroprotective effects of epoetin-b may be at least partly caused by the inhibition of calcineurin inhibitor-induced epithelial to mesenchymal transition by RHuEPO. Thus, correcting tissue hypoxia by raising Hb levels adds to the tissue protective effects of RHuEPO.…”
Section: Discussionmentioning
confidence: 99%
“…Indeed, survival rates remain quite stable, with only 50% of kidneys from deceased donors still functioning 10-year after transplant (1). The leading cause of allograft failures is chronic allograft nephropathy, a complex phenomenon characterized by progressive renal dysfunction, chronic interstitial fibrosis, tubular atrophy, vascular occlusive changes, and glomerulosclerosis (2,3). Many risk factors are known to influence longterm graft survival, such as recipient age, race, delayed graft function (DGF), HLA mismatching, and acute rejection episodes (4,5).…”
mentioning
confidence: 99%
“…23 Data from the literature also suggest that patients simultaneously displaying acute and chronic changes in their KAG, for example, interstitial infiltrate on a background of fibrosis, have worse subsequent KAG function and morphology. 6,26,32,33 Several other reasons can explain the absence of coordinated increase in urinary enzyme activity in patients with low GFR in this study. First, patients with acute tubular injury were excluded from the study.…”
Section: Discussionmentioning
confidence: 70%