RISK-FACTORS FOR VASCULAR-DISEASE AND ARTERIOVENOUS-FISTULA DYSFUNCTION IN HEMODIALYSIS-PATIENTS

Citation
S. Demarchi et al., RISK-FACTORS FOR VASCULAR-DISEASE AND ARTERIOVENOUS-FISTULA DYSFUNCTION IN HEMODIALYSIS-PATIENTS, Journal of the American Society of Nephrology, 7(8), 1996, pp. 1169-1177
Citations number
54
Categorie Soggetti
Urology & Nephrology
ISSN journal
10466673
Volume
7
Issue
8
Year of publication
1996
Pages
1169 - 1177
Database
ISI
SICI code
1046-6673(1996)7:8<1169:RFVAAD>2.0.ZU;2-A
Abstract
Vascular access dysfunction is an important cause of morbidity for dia lysis patients and a major contributor to hemodialysis cost. Thrombosi s is a leading cause of vascular access failure, and usually results f rom stenotic lesions in the venous outflow system. This study was desi gned to explore the impact of serum levels of various risk factors for thrombosis and accelerated fibrointimal hyperplasia on progressive st enosis, and the subsequent thrombosis of hemodialysis fistula. A cross -sectional and 2-yr prospective pilot study was performed in 30 nondia betic hemodialysis patients with primary arteriovenous fistula. Venous dialysis pressure, urea recirculation, color Doppler sonography, and angiography were used to monitor vascular access patency. Eleven patie nts (37%) developed a progressive stenosis in the venous circuit, whic h was complicated by thrombosis in three patients. Compared with the p atients without fistula dysfunction, these patients had higher serum l evels of monocyte chemoattractant protein-1 and interleukin-6, two cyt okines that regulate the proliferation of vascular smooth muscle cells , which is the key mechanism in the pathogenesis of fistula stenosis. In addition, they had hyperinsulinemia, hyperlipidemia, and increased plasma levels of two hemostasis-derived risk factors for thrombosis: p lasminogen activator inhibitor type 1 and factor VII. Monocyte chemoat tractant protein-1, interleukin-6, plasminogen activator inhibitor typ e 1, factor VII, triglycerides, and the ratios for cholesterol/HDL-cho lesterol, apolipoprotein (apo) A-I/apo, C-III, apo A-I/apo B, and gluc ose/insulin were independent predictors of fistula dysfunction. This s tudy demonstrates the influence of cytokines, hemostasis-derived vascu lar risk factors, hyperinsulinemia, and abnormalities of lipids and ap olipoproteins on primary fistula survival. The assessment of these fac tors might be useful for the identification of the patients at risk of fistula stenosis and thrombosis.