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• W2036355178 abstract "O421 Aims: Chronic allograft nephropathy (CAN) remains the most important cause of late renal graft loss. While accumulating evidence has elucidated both immunologic and non-immunologic factors which contribute to CAN, the mechanism by which graft dysfunction occurs and the processes involved in the development of CAN are not well understood. This study examined the role of microvascular injury in the development of CAN. Methods: We studied renal biopsies obtained from grafts with mild (n=30), moderate (n=27), and severe (n=22) CAN according to the Banff classification system. Microvascular injury was examined by light and electron microscopy, and immunohistochemistry for CD34. These findings were correlated with interstitial fibrosis (type I collagen), glomerular sclerosis (type IV collagen), and graft dysfunction (serum creatinine levels). Apoptotic dead cells were detected by the DNA nick end-labeling (TUNEL) method, and humoral and cellular immunity involved in CAN were studied by C4d, CD3 and GMP-17 staining. Results: CAN was characterized by progressive interstitial fibrosis, and the severity of CAN (defined by the Banff classification system) was correlated with graft dysfunction (r=0.81, p< 0.001). The CAN cases in the present study included chronic rejection (CR) (n=14, 17.8 %) and C4d-positive chronic humoral rejection (CHR) (n=6, 7.6 %). The development of CAN was characterized by injury to, and loss of identifiable peritubular capillaries (PTCs), accompanied with the development of renal scaring. These pathologic findings were found to be similar in all samples, irrespective of whether CR or CHR was observed. Morphologically, injured PTCs showed angioregressive changes which were characterized by decreased size, narrowing of the capillary lumen, the presence of TUNEL(+) dead cells, activated endothelial cells, detachment of endothelial cells from the basement membrane (BM), protrusion of endothelial cells into lumen, lamination of BM, and loss of PTCs. Importantly, a decrease in the number of PTCs significantly correlated with the development of interstitial fibrosis (r=-0.75, p< 0.001) and impairment of graft function (r=-0.69, p< 0.001). In the glomeruli, injured capillaries also showed angioregressive changes, similar to changes seen in injured PTCs. Additionally a decrease in the number of glomerular capillaries was significantly correlated with the development of glomerular sclerosis (r=-0.66, p<0.001), but not with graft dysfunction (r=0.36, p=0.16). Conclusions: Irrespective of whether CR, CHR or other factors lead to the development of CAN, the processes involved in its development appear similar, and are characterized by progressive injury and loss of renal microvasculature, with the development of renal scarring. Particularly, irreversible injury and loss of PTCs play a crucial role in the development of not only CAN, but also in the chronic deterioration of graft function." @default.
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• W2036355178 date "2004-07-01" @default.
• W2036355178 modified "2023-09-24" @default.
• W2036355178 title "INJURY AND SUBSEQUENT LOSS OF PERITUBULAR CAPILLARIES IN THE DEVELOPMENT OF CHRONIC ALLOGRAFT NEPHROPATHY" @default.
• W2036355178 doi "https://doi.org/10.1097/00007890-200407271-00434" @default.
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