title: Some old drugs improve late primary patency rate of native arteriovenous fistulas in hemodialysis patients.
abstract: Vascular access failure causes 20% of all hospitalizations of dialysis patients. Native arteriovenous fistulas, the best type of dialysis vascular access, have a 1-year primary patency rate that is extremely variable, ranging 40-80%. Neointimal hyperplasia is the most important cause of arteriovenous fistula late primary dysfunction. In recent years the arteriovenous fistula late primary patency rate has not improved because of the increase of old uremic patients with a high number of comorbidities and the lack of new therapeutic interventions. Therefore, we performed a long-term case-control study to analyze which factors or drugs may affect native arteriovenous fistula late primary patency rate in 60 incident hemodialysis patients. The arteriovenous fistula late primary patency rate was 75.1% after 12 months, 58.5% after 24 months, and 50% after 987 days. Homocysteine levels during follow-up had a significant direct association with vascular access failure (event vs. event-free 28.5+/-1.9 vs. 22.3+/-1.2 micromol/L, p<0.01). Folate values had a trend toward an inverse relationship with arteriovenous fistula failure (event vs. event-free 11.5+/-1.2 vs. 14.6 vs. 1.1 ng/mL, p=0.06). Patients treated with folic acid and/or statin had an arteriovenous fistula late primary patency rate significantly higher than patients without folic acid and statin therapy, respectively, 81.7% vs. 66% after 1 year and 71.5% vs. 39.1% after 2 years (p=0.02). Many other factors were not associated with vascular access failure. Statin and homocysteine-lowering folic acid therapy is associated with prolonged arteriovenous fistula survival. It is important to perform randomized trials to verify our observation.
authors.affiliation: Nephrology and Dialysis Unit, Vimercate Hospital, Vimercate 20059, Italy. righettim@hotmail.com
authors.forename: Marco
authors.initials: M
authors.lastname: Righetti
authors.forename: GianMichele
authors.initials: G
authors.lastname: Ferrario
authors.forename: Paola
authors.initials: P
authors.lastname: Serbelloni
authors.forename: Silvana
authors.initials: S
authors.lastname: Milani
authors.forename: Adalberto
authors.initials: A
authors.lastname: Tommasi
mesh_terms: D000368:Aged; D047228:Angiotensin II Type 1 Receptor Blockers / Q000627:therapeutic use; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D001166:Arteriovenous Shunt, Surgical / Q000009:adverse effects*; D015415:Biomarkers / Q000097:blood; D016022:Case-Control Studies; D019587:Dietary Supplements; D005492:Folic Acid / Q000627:therapeutic use*; D006083:Graft Occlusion, Vascular / Q000209:etiology / Q000503:physiopathology / Q000601:surgery*; D006710:Homocysteine / Q000097:blood; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D006965:Hyperplasia; D016015:Logistic Models; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use; D006435:Renal Dialysis; D018570:Risk Assessment; D012307:Risk Factors; D013997:Time Factors; D016896:Treatment Outcome; D014654:Vascular Patency / Q000187:drug effects*
chemical_list: D047228:Angiotensin II Type 1 Receptor Blockers; D000806:Angiotensin-Converting Enzyme Inhibitors; D015415:Biomarkers; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D010975:Platelet Aggregation Inhibitors; D006710:Homocysteine; D005492:Folic Acid