Abstract
Renal allograft rejection, represented by the wide spectrum of lesions with different pathogenesis, pathology patterns, clinical course and prognosis, still remains the most often cause of late graft dysfunction. Moreover, a combination of several factors, either of which may impact the post-transplant course, generally take place. We aimed to analyze the incidence of late renal allograft rejection variants, and to determine clinical factors and pathology features, influencing prognosis in the specific types of late renal allograft rejection. The data obtained from 361 patients with acute (n=227) or chronic (n=134) late allograft rejection (mean time after kidney transplantation 48.8 ± 46.1 months) were analyzed retrospectively. C4d expression was found in 34% cases of acute rejection and in 58% cases of chronic rejection (64% in chronic transplant glomerulopathy and 52% in transplant vasculopathy). 5-year graft survival comprised 48% and 24% for acute and chronic transplant rejection respectively (Р<0.01). Combination of acute cell-mediated rejection with chronic transplant rejection did not influence significantly the prognosis for the latter. Diffuse C4d expression on peritubular capillaries turned to be an independent prognostic factor regardless the pathology variant of renal allograft rejection. In contrast, focal C4d expression had no impact on the prognosis, which did not differ significantly from C4d-negative type. On the other hand, in acute rejection prognosis for C4dpositive forms was worse compared to C4d-negative (55% vs 25%; P <0.01), while in chronic rejection there was no difference between C4d-positive and C4d-negative forms (26% vs 24%; P=NS). In multivariate Cox-model analysis, the following factors appeared to influence the prognosis: presence of chronic transplant glomerulopathy, features of vasculitis, severity of tubulitis, presence of thrombotic micrioangiopathy and prominence of interstitial fibrosis.
Highlights
Since the advent of kidney transplantology as clinical discipline till days, graft rejection remains the major problem, hampering the results of transplantation
Depending on the dominant mechanism and the main site of injury, acute transplant rejection is subdivided into different variants: T-cellmediated rejection (TCMR) interstitial (Banff 1), TCMR vascular (Banff 2), vascular antibody-mediated rejection (AMR) with necrotizing arteritis (Banff 3) and acute AMR with microvascular bed involvement and subsequent evolution to the chronic AMR [4,5]
We aimed to analyze the incidence of the particular variants of late renal allograft rejection, evaluate their clinical presentation and course, and identify pathology and clinical prognostic factors for different types of late rejection
Summary
Since the advent of kidney transplantology as clinical discipline till days, graft rejection remains the major problem, hampering the results of transplantation. Despite of invention of new potent immunosuppressive agents, which substantially diminished the rate of acute rejection (mostly early episodes), the problem is not solved so far. Recent studies demonstrate that rejection remains the leading cause of late renal allograft losses [1,2,3]. Despite all above mentioned variants are clearly defined according to Banff-classification, quite often a combination of several mechanisms with different types graft damage occur simultaneously or consecutively, complicating Banff scoring and hampering the diagnosis [6,7,8]. The sequence and interconnectivity of events through time in mixed variants of rejection, as well as the prognostic value of each particular mechanism while both cell-mediated and antibodymediated immunity become activated, are still under discussion
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