The role of hyperparathyroidism, erythropoietin therapy, and CMV infection in the failure of arteriovenous fistula in hemodialysis.

Abstract

Vascular access failure is the main cause of morbidity in hemodialysis. Venous stenosis and subsequent thrombosis, as the result of intimal hyperplasia, is the major cause of vascular access failure. Intimal hyperplasia of the arteriovenous fistula (AVF) closely resembles the main histopathologic feature of atherosclerosis. In addition to the classic atherogenic risk factors, recently, cytomegalovirus (CMV) infection and parathyroid hormone (PTH) have been suggested as a potential cause of vascular disease. In the present study, we evaluated the relationship between AVF dysfunction and mean plasma PTH, cholesterolemia, high titer anti-CMV immunoglobulin G (IgG) (>250 U/mL), hematocrit, and mean erythropoietin (EPO) dose in 36 cases and 51 controls matched for age, time on dialysis, and type of AVF. A higher percentage of patients with AVF failure had a smoking habit and presented high anti-CMV IgG titer. Patients with AVF failure had significantly higher mean plasma PTH, whereas the groups did not differ for mean cholesterolemia and hematocrit. Mean EPO dose was slightly, but significantly, higher in the AVF failure group. Multiple logistic regression revealed that smoking, EPO dose, elevated mean plasma PTH and high titer anti-CMV antibodies, significantly increased the risk of AVF dysfunction. Our data suggest that hyperparathyroidism, smoking habits, CMV infection and EPO, independently of the hematocrit achieved, represent independent risk factors for hemodialysis access thrombosis.