Untitled - Roche Trasplantes

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EARLY DIAGNOSIS OF CHRONIC ALLOGRAFT NEPHROPATHY BY MEANS OF PROTOCOL BIOPSIES anti-Il2 receptor antibody (51). An alternative strategy has been studied since the early 1980’s, notably early conversion from a calcineurin inhibitor based regimen to one which eliminates the CNI after three, six or twelve months. It is not in the scope of this chapter to identify and review these studies which others have accomplished in formal metaanalyses (52, 53), but it is important to note that one of the more recent studies using sirolimus and corticosteroids as maintenance therapy was accompanied by protocol biopsies (54). In this study biopsies at implantation, 12 and 36 months were studied in a subset of patients that provided biopsy material at each time point. The most interesting feature of this study was that the group in which the CNI was eliminated had resolution of tubular atrophy between 12 and 36 months, without increased interstitial fibrosis. Thus the total CADI index of chronic damage was unchanged in the sirolimus treated patients, suggesting that the strategy might hold out some hopes for long term improvement in CAN, if effective and applicable clinical regimens can be developed to avoid the CNI’s. Future opportunities Clearly, very early diagnosis of events that may subsequently damage the graft might increase the effectiveness of interventions. The possibility that gene events will predict histology has been borne out in early studies from a number of groups including our own. Vitalone at the World Transplant Congress in Boston in July 2006 (55), presented data derived from Gene Microarrays demonstrating that genes associated with both CAN and rejection “turn on” –i.e., produce mRNA– earlier than the histological changes were apparent. If this is borne out in other laboratories and in other series of patients, it may offer a way of predicting the patients in whom intervention would be especially valuable. SUMMARY Chronic Allograft Nephropathy is the syndrome that has come to plague renal transplantation as the cause of most graft losses. It has been evident for as long as we have been transplanting the kidney, but in the early days it was overshadowed by acute rejection and mis-interpreted as an entirely immune related phenomenon termed “chronic rejection”. It has been the source of most concern to clinical transplant programs for the past ten years, but the long term nature of the syndrome has meant that it has not been an easy target for research. Paradoxically, the pharmaceutical industry –which has the most to gain from long term use of particular agents– is most unlikely to fund the research trials that we will need to prove which are the best treatment options. Long term investments in this area are likely to be superseded before they have produced any answers. We are thus left with the individual transplant centre studies, implied answers from long term cohort studies using older pharmaceutical agents and new molecular genomic and proteomic technologies that have yet to deliver on their promise. 25
BIOPSIA DE PROTOCOLO EN EL TRASPLANTE RENAL REFERENCES 1. Racusen LC, Solez K, Colvin RB, Bonsib SM, Castro MC, Cavallo T, et al. The Banff 97 working classification of renal allograft pathology. Kidney Int 1999; 55 (2): 713-23. 2. Chapman JR, O’Connell PJ, Nankivell BJ. Chronic Renal Allograft Dysfunction. JASN 2005; 16 (10): 3015-26. 3. Wilczek HE. Percutaneous needle biopsy of the renal allograft. A clinical safety evaluation of 1129 biopsies. Transplantation 1990; 50 (5): 790-97. 4. Furness PN, Philpott CM, Chorbadjian MT, Nicholson ML, Bosmans JL, Corthouts BL, et al. Protocol biopsy of the stable renal transplant: a multicenter study of methods and complication rates. Transplantation 2003; 76 (6): 969-73. 5. Schwarz A, Gwinner W, Hiss M, Radermacher J, Mengel M, Haller H. Safety and adequacy of renal transplant protocol biopsies. Am J Transplant 2005; 5 (8): 1992-6. 6. Vidhun J, Masciandro J, Varich L, Salvatierra O Jr., Sarwal M. Safety and risk stratification of percutaneous biopsies of adult-sized renal allografts in infant and older pediatric recipients. Transplantation 2003; 76 (3): 552-7. 7. Nankivell BJ, Borrows RJ, Fung CL, O’Connell PJ, Allen RD, Chapman JR. The natural history of chronic allograft nephropathy. N Engl J Med 2003; 349 (24): 2326-3. 8. Shapiro R, Randhawa P, Jordan ML, Shapiro R, Randhawa P, Jordan ML, et al. An analysis of early renal transplant protocol biopsies – the high incidence of subclinical tubulitis. Am J Transplant 2001; 1 (1): 47-50. 9. Nankivell BJ, Fenton-Lee CA, Kuypers DR, Cheung E, Allen RD, O’Connell PJ, et al. Effect of histological damage on long-term kidney transplant outcome. Transplantation 2001; 71 (4): 515-23. 10. Nicholson ML, Wheatley TJ, Doughman TM, White SA, Morgan JD, Veitch PS, et al. A prospective randomized trial of three different sizes of core-cutting needle for renal transplant biopsy. Kidney Int 2000; 58 (1): 390-5. 11. Furness PN, Taub N. International variation in the interpretation of renal transplant biopsies: report of the CERTPAP Project. Kidney Int 2001; 60 (5): 1998-2012. 12. Gough J, Rush D, Jeffery J, Nickerson P, McKenna R, Solez K, et al. Reproducibility of the Banff schema in reporting protocol biopsies of stable renal allografts. Nephrol Dial Transplant 2002;17 (6):1081-84. 13. Veronese FV, Manfro RC, Roman FR, Edelweiss MI, Rush DN, Dancea S, et al. Reproducibility of the Banff classification in subclinical kidney transplant rejection. Clin Transplant 2005; 19 (4): 518-21. 14. Sis B, Dadras F, Khoshjou F, Cockfield S, Mihatsch MJ, Solez K. Reproducibility studies on arteriolar hyaline thickening scoring in calcineurin inhibitor-treated renal allograft recipients. Am J Transplant 2006; 6: 1444-50. 15. Briganti EM, Russ GR, McNeil JJ, Atkins RC, Chadban SJ. Risk of renal allograft loss from recurrent glomerulonephritis. New Eng J Med 2002; 347: 103-9. 16. Nankivell BJ, Chapman JR, Gruenewald SM. Detection of chronic allograft nephropathy by quantitative doppler imaging. Transplantation 2002: 74: 90-6. 26
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