Ruolo delle alterazioni emocoagulative nella genesi della trombosi dell'accesso vascolare nell'uremico cronico in emodialisi

Vascular access dysfunction is an important cause of morbidity for dialysis patients and a major contributor to hemodialysis cost. Thrombosis is a leading cause of vascular access failure, and usually results from stenotic lesions in the venous outflow system. We sought to explore the impact of serum levels of various risk factors for thrombosis and accelerated fibrointimal hyperplasia on progressive stenosis, and subsequent thrombosis of hemodialysis fistula. A cross-sectional and two-year prospective pilot study was performed in 30 nondiabetic hemodialysis patients with primary arteriovenous fistula. Venous dialysis pressure, urea recirculation, colour Doppler sonography and angiography were used to monitor vascular access patency. Eleven patients (37 percent) developed a progressive stenosis in the venous circuit, which was complicated by thrombosis in three patients. Compared to the patients without fistula dysfunction, these patients had higher serum levels of monocyte chemoattractant protein-1 and interleukin-6, two cytokines that regulate the proliferation of vascular smooth muscle cells, which is the key mechanism in the pathogenesis of fistula stenosis. In addition, they had hyperlipidemia, and increased plasma levels of two hemostasis-derived risk factors for thrombosis: plasminogen activator inhibitor type 1 and factor VII. Monocyte chemoattractant protein- 1, interleukin-6, plasminogen activator inhibitor type 1, factor VII, triglycerides, and the ratios cholesterol/HDL-cholesterol, apo A-I/apo C-III and ape A-I/apo B were independent predictors of fistula dysfunction. This study demonstrates the influence of cytokines, hemostasis-derived vascular risk factors and abnormalities of lipids and apolipoproteins on primary fistula survival. The assessment of these factors might be useful for the identification of the patients at risk of fistula stenosis and thrombosis.