Histopathological diagnosis of acute and chronic rejection in pediatric kidney transplantation

Abstract

ABO-compatible as well as ABO-incompatible kidney transplantation are well established in the pediatric population. There are particularities in the histopathological evaluation of pediatric kidney transplant biopsies as for example the recurrence of certain diseases different from the adult population. Furthermore, the challenging transition of pediatric renal transplant recipients to adulthood is associated with an increased rate of non-adherence triggered rejection episodes. With modern immunosuppressive drugs, T-cellmediated rejection of renal allografts is well controlled. In contrast, antibody-mediated rejection (AMR) is increasingly recognized as one of the major reasons for allograft loss. However, the 2001 diagnostic Banff criteria for antibodymediated rejection require further refinement, as the morphological spectrum of AMR expands while effective therapeutic strategies are lacking. For example, endarteritis, which traditionally has been attributed to T-cell-mediated rejection, has recently been shown to be part of the AMR spectrum in some cases. Many findings in transplant renal biopsies are not specific for a certain disease but need consideration of differential diagnoses. To use the term "chronic allograft nephropathy" as a diagnostic entity is no longer appropriate. Therefore, the precise identification of specific diseases is paramount in the assessment of transplant renal biopsies in order to enable tailored therapeutic management.

Longitudinal evaluation of perfusion changes in acute and chronic renal allograft rejection using arterial spin labeling in translational mouse models

“…In the chronic allograft rejection model, severe and permanent perfusion impairment was observed 3 and 6 weeks after transplantation, while renal perfusion in isografts without rejection following short CIT of 30 minutes had recovered to baseline conditions at that timepoint. Severe and permanent perfusion impairment in allografts could be explained by severe histological alterations, including microcirculatroy lesions in addition to interstitial inflammation and fibrosis consistent with chronic renal allograft rejection . Discrimination between isografts without rejection and allografts was even better compared to the acute model, potentially due to the microcirculatory lesions associated with vascular occlusion due to endothelialitis.…”

Acute cellular rejection treatment outcomes stratified by Banff grade in pediatric kidney transplant

“…Our center's approach will treat all patients with Banff IB with rATG. Patients with Banff II and III have been reported to experience steroid‐resistant rejection and increased risk for graft loss . Thirty percent (four out of 13) of patients with Banff II rejection in our study received pulse steroids only while all patients with Banff III received rATG.…”

“…Patients with Banff II and III have been reported to experience steroid-resistant rejection and increased risk for graft loss. 10,11 Thirty percent (four out of 13) of patients with Banff II rejection in our study received pulse steroids only while all patients with Banff III received rATG. Of these four, one had medical contraindications precluding treatment with rATG.…”

Association Between Promoter Polymorphisms in CD46 and CD59 in Kidney Donors and Transplant Outcome

“…A potential explanation for the opposite effect of this SNP in kidney and lung transplantation could apply to the timing of the effect and the fact that acute and chronic rejection (including BOS) are two distinct entities ( 43 – 45 ). Chronic rejection is a much more multifactorial process requiring multiple hits, resulting in gradual parenchymal fibrosis and obliterative vasculopathy and progressive graft dysfunction ( 43 , 46 ), whereas acute rejection is identified by cellular and humoral attack resulting in rapid graft damage when untreated ( 43 , 47 ). In our kidney transplant cohort, the observed effect of the CD59 promoter SNP occurred in the first weeks posttransplantation without an effect thereafter.…”