Abstract
Introduction:Renal fibrosis is the end point of a process that begins at transplant, with ischemia reperfusion and early inflammation, and progresses over time with immunological and non-immunological phenomena. Early identification of morphological markers and intervention could improve graft function and survival.Objective:to evaluate the correlation between intensity and specificity of pre-transplant anti-HLA antibodies and kidney allograft pathology in order to identify early risk factors or markers of allograft dysfunction.Methods:A retrospective cohort of kidney transplant recipients with pre-transplant anti-HLA antibodies who underwent graft biopsy within the first two years post-transplant was divided into two groups according to the specificity of anti-HLA antibodies: nonspecific (non-DSA, n = 29) and specific (DSA+, n = 16). Kidney graft pathology, renal function, and proteinuria were analyzed.Results:general characteristics were similar in both groups, except for the higher dose of thymoglobulin in DSA+ group (p < 0.05). The non-DSA group had higher scores for glomerulosclerosis, interstitial inflammation (i) and interstitial fibrosis (ci) (p < 0.05) and higher incidence of cell-mediated acute rejection. No statistical difference in incidence of antibody-mediated rejection, renal function, and proteinuria was observed during follow up.Discussion and conclusions:the difference in inflammation scores and interstitial fibrosis may be associated to the higher incidence of acute cell-mediated rejection and polyomavirus nephropathy in the Non-DSA group. We also should take into account the protective effect of higher doses of thymoglobulin, reducing ischemia reperfusion injury in the DSA+ group. The short follow-up might have been insufficient to detect long-term changes in allograft tissue, renal function, and proteinuria.
Highlights
Renal fibrosis is the end point of a process that begins at transplant, with ischemia reperfusion and early inflammation, and progresses over time with immunological and non-immunological phenomena
The aim of this study was to evaluate the correlation between intensity and specificity of preformed anti-human leukocyte antigen (HLA) antibodies and renal pathology in graft biopsies performed within the first two years after renal transplantation, in order to identify risk factors potentially associated with the onset of graft fibrosis and early clinical outcomes
Eleven patients (40%) in the donor-specific antibodies (DSA) group and thirtythree patients (53%) in Non-DSA group were excluded because they had no graft biopsy performed (p = 0.28)
Summary
Renal fibrosis is the end point of a process that begins at transplant, with ischemia reperfusion and early inflammation, and progresses over time with immunological and non-immunological phenomena. Discussion and conclusions: the difference in inflammation scores and interstitial fibrosis may be associated to the higher incidence of acute cell-mediated rejection and polyomavirus nephropathy in the Non-DSA group. The fibrosis process begins throughout the first year post-transplant, especially within the first three months, triggered by self-limiting inflammation secondary to reperfusion injury and maintained by continuous inflammatory immune response that facilitates progression of renal disease[2,3] Several factors are involved in the intensity and extent of fibrosis, such as donor age, donor source (living vs deceased), and cold and warm ischemia times. A higher score of IF/TA in the graft biopsy is associated with worse renal function, with a negative impact on graft survival
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