They are useful for detecting subclinical rejection, recurrent disease, drug toxicity and polyomavirus nephropathy. Current literature mainly discusses the significance of subclinical rejection during the early post-transplant period. It has been suggested that protocol biopsies performed within the first year after kidney transplantation for the detection and treatment of subclinical rejection may be a major factor in preserving long-term graft function.[1-3] However, the benefit of long-term allograft biopsies is largely unproved, and the strategy is yet to be widely implemented. The recent progress in immunosuppressive agents has considerably
improved renal allograft survival, GSI-IX with 5-year graft survival now exceeding 90%.[4] In addition, the prevalence of subclinical rejection has decreased over time in accordance with the development of new immunosuppressant drugs. Rush et al.[5] reported a randomized, prospective, multicentre study that used tacrolimus, mycophenolate mofetil and steroid as the baseline regimen, in which the overall prevalence of subclinical rejection between months 1 and 6 was only 4.6%. In contrast, in recent years, some reports have been published
about post-transplant recurrence of primary glomerulonephritis.[6-10] Also, calcineurin inhibitor (CNI) nephrotoxicity remains one of the most difficult issues associated with chronic allograft damage.[11-13] In this respect, the utility of long-term protocol biopsy may be of clinical significance for the detection of graft dysfunction learn more as a result of non-immune factors, such as CNI nephrotoxicity
and recurrence of glomerulonephritis, rather than subclinical rejection. This review discusses the value of long-term protocol biopsies after kidney transplantation focusing on the issue of immunological and non-immunological factors. Early detection and treatment of subclinical rejection improves outcome. However, reported incidence rates of subclinical rejection differ widely, varying from 1% to 45% in the first 3–6 months post transplantation.[1, 2, 14-16] Some reasons for the differences in reported subclinical Y-27632 chemical structure rejection rates include variation in human leukocyte antigen (HLA) matching, the incidence of delayed graft function, and the immunosuppressive protocol used.[2] Also, the difference can be explained in part by the inclusion of borderline changes, use of different inclusion criteria, and different timings of the biopsies. Comparisons between studies are complicated further by the fact that some studies include small numbers of patients and precise inclusion criteria are not reported. The treatment of subclinical rejection is a difficult problem with no easy answer. Commonly, patients with biopsies showing borderline changes or T-cell–mediated rejection were treated with corticosteroid bolus alone or thymoglobulin in combination with steroid.