Abstract: Objective Recently, some researchers found that venous neointimal hyperplasis existed before AVF operation in ESRD patients. We explored the mechanism of the venous neointimal hyperplasis. Methods We screened out 8 patients with venous neointimal hyperplasis during the first AVF operation (the AVF operation group), and 8 patients with venous neointimal hyperplasis during ateriovenous fistula repair operation (the AVF repair group). Venous samples were subjected to immunohistochemistry for the expression of smooth muscle actin (SMA), vimentin, desmin and a disintegrin-like and metalloproteinase with thrombospondin
type l motifs-1 (ADAMTS1) to explore the mechanism of venous neointimal hyperplasis. Result In the AVF operation group, most cells in the hyperplastic neointima layer were myofibroblasts with SMA+, vimentin+ and desmin-, and a few cells were contractile smooth cells with SMA+, vimentin- and desmin+. In the
AVF repair group, almost all cells in the hyperplastic neointima layer were myofibroblasts with SMA+, vimentin+, and desmin-. ADAMTS1 staining was negative in the AVF operation group and was positive in one venous sample in the AVF repair group. Conclusion Myofibroblasts play an important role in the neointimal
hyperplasis before AVF operation in ESRD patients. Blocking the phenotypic transformation and migration of smooth muscle cells may be an effective way to cure the neointimal hyperplasis.

Key words: ESRD, arteriovenous fistula stenosis, neointimal hyperplasis, smooth muscle phenotype