The authors reply.

We would like to thank Drs. Eroglu and Kocyigit for their comment on possible use of colchicine on arteriovenous fistula maturation via neointimal hyperplasia blockage.[1] We used simvastatin because it is a pleiotropic molecule capable of modulating the gene expression of vascular endothelial growth factor-A and matrix metalloproteinase-9. In our studies, simvastatin treated vessels had improved vascular remodeling in a experimental murine model of arteriovenous fistula (AVF) with chronic kidney disease using a clinical dose [2]. As pointed out by Eroglu and Kocyigit, simvastatin is associated with rhabdomyolysis, hepato-toxicity, and uremia induced cardiomyopathy [3]. Taking this into consideration, we have begun to consider local delivery of simvastatin to the vessel wall using nanoparticles or alginate gel wraps to decrease these side effects.

Colchicine treatment for six months has been shown recently to decrease in stent restenosis in patients with coronary disease treated with bare metal stents [4]. This is felt to be because of its ability to inhibit microtubule formation as well as an anti-inflammatory component [5]. Furthermore, it is interesting that a trial using colchicine was negative in patients undergoing angioplasty of coronary arteries while a separate trial in patients undergoing stent placement was positive [4, 6]. The mechanism for this observation may be due to elastic recoil, which occurs in the artery after angioplasty and also in the vein. In conclusion, we think colchicine is a plausible therapy, which may reduce venous neointimal hyperplasia in patients with hemodialysis vascular access, and further studies using this molecule need to be performed to determine its efficacy.