Subclinical Rejection: a Universally Held Concept?
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KIDNEY TRANSPLANTATION (M HENRY AND R PELLETIER, SECTION EDITORS)
Subclinical Rejection: a Universally Held Concept? David N. Rush 1
# Springer Nature Switzerland AG 2020
Abstract Purpose of Review The goal of this paper is to evaluate the published literature to assess the evidence for a pathogenic role for subclinical inflammation in the renal allograft. Recent Findings It has become apparent from a growing body of evidence that most of the inflammation observed in renal allografts is alloimmune in nature, and ultimately pathogenic, even if it is below the classic Banff threshold for rejection. Summary There are recent data to indicate the subclinical inflammation that is usually detectable only by protocol biopsies is a risk factor for subsequent clinical T cell–mediated rejection, the development of de novo donor-specific antibody (DSA), and graft loss. The need and potential for novel non-invasive methods in the detection of subclinical inflammation in the renal allograft are discussed in the context of future research studies. Keywords Subclinicalrejection . Renaltransplantation . Non-invasive diagnosis . Urine chemokines . Urine metabolomics . Gene expression profiles
Introduction The term “subclinical rejection” was coined to refer to the finding of Banff criteria for acute rejection in wellfunctioning renal allografts in biopsies performed routinely at set times post-transplant [1]. It should be recalled that the current Banff criteria for acute rejection resulted from the merging of the original Banff classification, published in 1993 [2], and those of the National Institutes of Health Cooperative Clinical Trials in Transplantation (CCTT) [3]. This collaboration was published in 1999 [4] and remains the standard for the diagnosis of T cell–mediated rejection (TCMR). The threshold for TCMR in Banff was arbitrarily set at ai2at2, which corresponds to inflammation in at least 25% of the renal interstitium and between five and nine lymphocytes in the renal tubules, respectively (Banff I A); the inflammation was restricted to the non-atrophic parenchyma. The CCTT criteria were less stringent than those in Banff, and lesser degrees of inflammation were considered as rejection. This article is part of the Topical Collection on Kidney Transplantation * David N. Rush [email protected] 1
Rady Faculty of Health Sciences Centre, University of Manitoba, 820 Sherbrook Street, Winnipeg, MB R3A 1R9, Canada
Importantly, there was no specified degree of renal dysfunction that was required for the diagnosis of TCMR in Banff, but the biopsy had to be “clinically indicated”—i.e., usually for a rise in the serum creatinine of at least 20%. Notably, in CCTT, the clinical and pathological criteria for TCMR were found to be no different with rises in serum creatinine between 5 and 30% [3].
Subclinical Rejection in Patients Treated with Cyclosporine In our first paper, we described varying degrees of inflammation, from “borderline” rejection to Banff I A and Banff II A, in biopsies obtained at post-transplant months 1, 2, and
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