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NDT Advance Access published online on April 2, 2008
Nephrology Dialysis Transplantation, doi:10.1093/ndt/gfn130
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© The Author [2008]. The online version of this article has been published under an open access model. Users are entitled to use, reproduce, disseminate, or display the open access version of this article for non-commercial purposes provided that: the original authorship is properly and fully attributed; the Journal and Oxford University Press are attributed as the original place of publication with the correct citation details given; if an article is subsequently reproduced or disseminated not in its entirety but only in part or as a derivative work this must be clearly indicated. For commercial re-use, please contact journals.permissions@oxfordjournals.org


Chronic allograft nephropathy—clinical guidance for early detection and early intervention strategies

Daniel Serón1, Wolfgang Arns2 and Jeremy R. Chapman3

1 Nephrology Department, Hospital Universitario de Bellvitge, Barcelona, Spain 2 Cologne General Hospital, Merheim Medical Centre, Koeln-Merheim, Germany 3 Centre for Transplant and Renal Research, University of Sydney, Westmead Hospital, Westmead, New South Wales, Australia

Correspondence and offprint requests to: Jeremy R. Chapman, Director of Acute Internal Medicine, Centre for Transplant and Renal Research, Millennium Institute, University of Sydney, Westmead Hospital, Westmead, NSW 2145, Australia. Tel: +61-2-9845-6349; Fax: +61-2-9845-8300; E-mail: Jeremy_Chapman@wsahs.nsw.gov.au

Keywords: chronic allograft nephropathy; everolimus; proliferation signal inhibitors/mammalian target of rapamycin (mTOR) inhibitors; renal transplantation; sirolimus

The first 150 words of the full text of this article appear below.



   Introduction
 
Improvements in reducing acute rejection rates following kidney transplantation in the last decade have not been mirrored by improvements in long-term graft survival rates [1,2]. One of the major causes of late graft loss in renal transplant recipients is chronic allograft nephropathy (CAN) [3–5] (Figure 1). CAN is highly prevalent in renal transplant recipients, with moderate to severe CAN present in 24.7% of recipients at 1 year post-transplant and in 89.8% of recipients by 10 years post-transplant [6]. CAN is defined by the histopathological features of interstitial fibrosis and tubular atrophy, but can also be associated with subclinical rejection, transplant glomerulopathy [6–8] or transplant vasculopathy caused by smooth muscle cell proliferation [4,9]. Therefore, the term CAN is being employed quite widely to describe a clinical syndrome instead of defining the presence of interstitial fibrosis or tubular . . . [Full Text of this Article]

Clinical guidance-—early detection before CAN becomes established
Clinical guidance—early intervention through identification of risk factors before CAN occurs


   Conclusions
 

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