Risk factors for vascular disease and arteriovenous fistula dysfunction in hemodialysis patients.
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. This study was designed to explore the impact of serum levels of various risk factors for thrombosis and accelerated fibrointimal hyperplasia on progressive stenosis, and the subsequent thrombosis of hemodialysis fistula. A cross-sectional and 2-yr prospective pilot study was performed in 30 nondiabetic hemodialysis patients with primary arteriovenous fistula. Venous dialysis pressure, urea recirculation, color Doppler sonography, and angiography were used to monitor vascular access patency. Eleven patients (37%) developed a progressive stenosis in the venous circuit, which was complicated by thrombosis in three patients. Compared with 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 hyperinsulinemia, 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 for cholesterol/HDL-cholesterol, apolipoprotein (apo) A-I/ apo C-III, apo A-I/apo B, and glucose/insulin were independent predictors of fistula dysfunction. This study demonstrates the influece of cytokines, hemostasis-derived vascular risk factor, hyperinsullnemia, and abnormallties 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.
De Marchi
S
S
Department of Internal Medicine, University of Udine Medical School, Italy.
Falleti
E
E
Giacomello
R
R
Stel
G
G
Cecchin
E
E
Sepiacci
G
G
Bortolotti
N
N
Zanello
F
F
Gonano
F
F
Bartoli
E
E
D000368:Aged; D001166:Arteriovenous Shunt, Surgical / Q000009:adverse effects*; D001779:Blood Coagulation Factors / Q000032:analysis; D001786:Blood Glucose / Q000032:analysis; D018932:Chemokine CCL2 / Q000097:blood; D015897:Comorbidity; D003430:Cross-Sectional Studies; D016207:Cytokines / Q000097:blood; D005260:Female; D005352:Fibromuscular Dysplasia / Q000097:blood / Q000453:epidemiology* / Q000209:etiology; D006801:Humans; D006946:Hyperinsulinism / Q000453:epidemiology; D006949:Hyperlipidemias / Q000453:epidemiology; D006973:Hypertension / Q000453:epidemiology; D015850:Interleukin-6 / Q000097:blood; D007676:Kidney Failure, Chronic / Q000097:blood / Q000453:epidemiology / Q000628:therapy; D008055:Lipids / Q000097:blood; D008297:Male; D008875:Middle Aged; D009765:Obesity / Q000453:epidemiology; D010865:Pilot Projects; D017395:Plasminogen Activator Inhibitor 1 / Q000032:analysis; D010982:Platelet-Derived Growth Factor / Q000032:analysis; D011446:Prospective Studies; D006435:Renal Dialysis; D012307:Risk Factors; D012907:Smoking / Q000453:epidemiology; D013927:Thrombosis / Q000097:blood / Q000453:epidemiology* / Q000209:etiology
D001779:Blood Coagulation Factors; D001786:Blood Glucose; D018932:Chemokine CCL2; D016207:Cytokines; D015850:Interleukin-6; D008055:Lipids; D017395:Plasminogen Activator Inhibitor 1; D010982:Platelet-Derived Growth Factor