Abstract

Background: Chronic transplant glomerulopathy is one of chronic lesions
developing secondary to chronic, or repetitive injury to glomerular endothelium. It may occur in a response to humoral rejection, cellular rejection or thrombotic microangiopathy. There is limited data about histological and clinical characteristics of that lesion including its impact on graft survival. The aim of the study: to clinically and histologically characterize TG and its impact on graft survival.
Material/Methods: We retrospectively analyzed all 152 cases of chronic transplant glomerulopathy recognized in Transplantation Institute since 1996, and compared it with 86 non-TG cases matched for the stage of advancement of other chronic lesions, such as interstitial fibrosis, tubular atrophy, arteriosclerosis and arteriolar hyalinization. In both TG, and control group all the biopsies were performed due to slow rise in serum creatinine concentration and/or recent onset of proteinuria.
Results: In comparison to control TG was associated with significantly lower
survival rate (83% vs. 49%, p<0.0001) higher incidence of proteinuria (34% vs. 88%, p<0.0001), and higher incidence of HCV infection (45% vs. 33%, p=0.0033). There was no difference in max and last PRA values, nor number of HLA mismatches between TG, and non-TG patients. Morphological analysis
(Banff 07 classification) revealed significantly higher incidence of C4d deposition in PTC (77% vs. 1%, p<0.0001), and glomeruli (66% vs. 0%,
p<0.0001), as well as an acute transplant glomeurlopathy (14% vs. 0%, p<0.0001) and endarteritis ("v", 9% vs. 0%, p=0.005). Banff scores for inflammatory infiltrates ("i" and "ti" score), and PTC-itis were significantly higher in TG biopsies in comparison to control (p<0.005 in each parameter).
Conclusions: Chronic transplant glomerulopathy is associated with poorer graft survival and higher proteinuria than other chronic kidney transplant lesions. In substantial percentage of cases TG is associated with C4d deposition in both PTC and glomerular capillaries, and co-occurrence of inflammatory interstitial and vascular infi ltrates which is in contrast to other common chronic lesions in kidney graft.

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