Background. The contribution of the hemodialysis (HD) vascular access type to inflammation is unclear. Methods. We conducted a prospective observational study in an incident HD population. C-reactive protein (CRP), interleukin-6 (IL-6), and interferon-γ-induced protein (IP-10) were measured before and at 6-time points after access placement for 1 year. Results. Sixty-four incident HD patients were included (tunneled catheter (TC), , arteriovenous fistula (AVF), , and arteriovenous graft (AVG), ). A mixed effects model was performed to adjust for age, sex, race, coronary artery disease, diabetes mellitus, infections, access thrombosis, initiation of HD, and days after access surgery. In comparison to AVFs, the presence of a TC was associated with significantly higher levels of CRP ( ), IL-6 ( ), and IP-10 ( ). The presence of an AVG was associated with increases in CRP ( ) and IP-10 ( ). Conclusions. Patients who initiate HD with a TC or an AVG have a heightened state of inflammation, which may contribute to the excess 90-day mortality after HD initiation. 1. Introduction The most recent 2009 USRDS report observed high first- and second-month death rates after HD initiation [1]. The type of HD vascular access is significantly associated with risk of death. The CHOICE study reported 50% higher mortality rates in patients initiating HD with a TC as compared to patients with an AVF. There was a trend toward higher mortality rates (21% increased) in incident HD patients with an AVG compared to those with an AVF; however this did not achieve statistical significance [2]. A recently published Canadian study in 40,526 incident dialysis patients reported an 80% higher 1-year mortality for HD patients with a TC compared to PD patients and HD patients with an AVF or AVG [3]. Potential reasons for these findings include the higher rate of infection and sepsis associated with TCs, relative to AVFs; however the contribution of the vascular access type, independent of infection, may also be a factor. The prevalence of chronic inflammation is high (35–65%) in the chronic kidney disease (CKD) and end-stage renal disease (ESRD) populations [4–7]. Inflammation, as assessed by using C-reactive protein (CRP) level, is a strong predictor of all-cause and cardiovascular mortality in ESRD patients [5–9]. Multiple clinical factors and intercurrent clinical events may contribute to inflammation [10–14]. Studies analyzing the relationship between TCs and CRP levels have reported contradictory findings. Although several small studies reported an association between TCs and
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