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Increased expression od TGF-B and vimentin in stenotic lesions of early artetio-benous fistula failure in patients with chronic kidney disease

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Backgrounds: Hemodialysis remains the most frequent therapeutic procedure in the treatment of terminal stage of chronic kidney disease (CKD). The primary arteriovenous (AV) fistula is widely accepted as the best permanent vascular access. Early fistula failure defined as non matured or failed fistula within three months after its creation appears in 25-60% of all created fistulas. The pathogenesis of early fistula failure is not very well understood. Many general and local factors are involved: patient’s age, sex, primary renal disease, small vessel’s diameter, presence of accessory veins, prior venipunctures, surgical skill, genetics, etc. Histological investigations have confirmed the neointimal venous hyperplasia as a major pathological finding in stenotic lesions of AVF failure, due to local inflammation, oxidative stress and migration and proliferation of myofibroblast, fibroblast and endothelial cells.

Materials and methods: A total of 89 patients with stadium 4-5 of CKD are involved in the study. A typical radio-cephalic AVF is created in all patients. Part of fistula vein was taken for histology (H&E, van Gieson), immunohistiochemical (Vimentin, TGF-beta and KI67) and morphometric analysis. The investigations were repeated after fistula failure in the same vein proximally (observational point 2). A appropriate statistical method was applied.

Results: 31 patients developed early AVF failure. We found increased expression in Vimentin and TGB β in all patients even before AVF creation, but there were no statistical differences between the patients with the early AVF failure and functional AVF. But, when we compared the results from the second point, after AVF failure, we found significant increase in both markers. We didn’t find any expression of KI 67. We also found significant luminal stenosis in the veins that has increased after AVF failure.

Conclusion: Neointimal hyperplasia and medial hypertrophy are present in veins of CKD patients before AVF creation and they increase after its creation. The dominant cells within the stenoses veins are myofibroblasts. The increased presence of TGF β in failed AVF confirms the possible role of inflammation and oxidative stress in the development of neointimal hyperplasia. Abbrevations: CKD – Chronic Kidney Disease, AVF – Arterio – Venous Fistula, IH – Intimal Hyperplasia, H&E – Haematoxylin and Eosin

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