RESUMO
Background: vascular access thrombosis in patients on maintenance hemodialysis [HD] is an important morbidity factor. Arterial or venous thrombotic events have been described as complications in patients on regular HD and positive titers of anticardiolipin antibodies [ACAs]. ACAs are commonly found in patients with chronic hepatitis C viral [HCV] infection but their pathogen etic role and the mechanisms that stimulate their production have not yet been clarified. In HCV infection, ACAs are generally cofactor independent and may represent an epiphenomenon of the infection. Some studies, however, have found an increased incidence of thrombotic disorders in patients with chronic HCV infection who manifest ACAs positivity suggesting that the presence of these autoantibodies may predispose to thrombosis in specific HCV-infected patients
Aim of the work: this study was designed to evaluate the prevalence of ACAs associated with chronic HCV infection in chronic HD patients and its possible relation to recurrent arterio-venous fistula thrombosis [A VFT]
Patients and methods: eighty-four out of 97 patients undergoing chronic outpatient HD treatment in a single dialysis facility, who had a functional autologus A VF, were offered enrollment in the study. All baseline data collection occurred during December 2003, with follow-up through December 2005. Nonfasting pre-HD blood samples were collected for determination of serum levels of creatinine, glucose, albumin, and total cholesterol, and blood urea nitrogen levels. Fractional clearance index for urea [Kt/v] was calculated monthly. Standardized enzyme-linked immunosorbent assay [ELISA] was considered positive [medium to high titre] for lgG ACA with any value > 40 units. High sensitivity C reactive protein [hs-CRP] was measured by latex-enhanced turbidometry. Antibodies to HCV [HCV ab] were investigated using lnnotest TM HCV Ab IV ELISA 3rd generation. Vascular access failure was defined as loss of bruit or thrill and/or sudden cessation of function of the A VF rendering HD impossible. By the end of follow up period [median of 16 months], data were collected and statistically analyzed
Results: thirty four/84 [41%] patients experienced recurrent AVFT during follow-up versus 50/84 [59%] who did not. Higher mean baseline lgG-ACAs levels [i.e > 40 units] were noticed in those patients who subsequently thrombosed their fistulae compared with who did not [22/34 [65%] versus 10/50 [20%], P<0.001]]. Correlation analyses revealed that the incidence of recurrent A VFT were associated with HCV positivity 30/34 [88%], P =0.04] as well as plasma serum levels of hs CRP 21/34 [62%], P = 0.03], but not with age, gender,· serum albumin, months on dialysis, creatinine, current smoking, hypertension, hypercholesterolemia, or the Kt/v .The prevalence of HCV positivity was 65/84 [77.4%]. The incidence of recurrent AVFT was found to be higher among the group of patients having ACA+ve and HCV +Ve 19/34 [56%] compared with who had no recurrent AVFT within the same group of patients 8/50 [16%] [P<0.001]
Conclusion: from this study, it can be concluded that a possible relationship does exist between chronic HCV infection associated ACAs and recurrent AVFT in chronic HD patients. Whether this is a true association or a mere coincidence remains to be determined. This is a single-center study with a limited number of patients and should be confirmed by other mutlicenter prospective controlled trials with larger numbers of patients