Abstract
Aggressive NIH is a common histopathological lesion found at the sites of venous stenosis in arteriovenous fistula (AVF) and arteriovenous grafts (AVG). Inflammatory mediators have been proposed to play a pathogenic role in NIH, but there is paucity of data evaluating this hypothesis in clinical studies or in animal models. Serum levels of inflammatory mediators can potentially identify patients at high risk of AVF and AVG dysfunction. In a cross-sectional cohort study of 754 HD patients who were part of the NIED study cohort, we examined the associations between inflammatory markers including serum interleukin (IL) 1β, IL-6, C-reactive protein (CRP), and tumor necrosis factor-α (TNF-α) and type of vascular access. Unadjusted and multivariate-adjusted linear regression models were used. In addition, time-dependent regression model was used to assess the association between inflammatory markers and mortality. We observed that in the multivariate-adjusted model, inflammatory mediators interleukin-6 (IL-6), interleukin-1L-ß (IL-1ß), and C-reactive protein (CRP), the predicted value in hemodialysis patients, are lowest in patients with AVF and highest in central venous catheter (CVC) and AVG even in case-mix and malnutrition-inflammation complex syndrome (MICS)-adjusted models. IL-6 and CRP levels fall consistently in the same patients when AVG or CVC is changed to AVF and increase if the same patient changes access from AVF to AVG or CVC. Obesity is a risk factor for fistula failure and fistulas are associated with the lowest mortality compared with CVC and AVG. We did not find any statistically significant association between tumor necrosis factor-α (TNF- α) and vascular access outcomes. Higher levels of inflammatory mediators seen in CVC and AVG compared with AVF could potentially explain the higher mortality seen in patients with CVC and AVG compared with AVF.
Highlights
Stenosis frequently occurs in the venous segment of the arteriovenous fistula (AVF) most commonly due to neointimal hyperplasia (NIH) and at the vein-graft anastomosis (VGA) in arteriovenous grafts (AVG), impeding flow frequently resulting in failure (8–14)
Inflammatory mediators have been proposed to play a pathogenic role in NIH in both AVF and AVG, but the role they play both as predictors of access failure as well as their pathogenic role in NIH is not clearly understood
Inflammatory markers, we found that some inflammatory mediators (IL-6 and IL-1ß) were significantly higher in patients with central venous catheter (CVC) compare with patients with AVF even in case-mix and MICSadjusted models
Summary
Inflammatory mediators have been proposed to play a pathogenic role in NIH in both AVF and AVG, but the role they play both as predictors of access failure as well as their pathogenic role in NIH is not clearly understood. Vascular calcification and inflammation are intricately linked Inflammatory mediators such as TNF-alpha can induce mineralization of calcifying vascular cells in vitro and calcium phosphate crystals could activate human monocyte-derived macrophages inducing a proinflammatory state via protein kinase C and MAP kinase pathways (17,18). This vicious cycle of inflammation and arterial calcification (likely more in AVG than AVF) could explain the association between inflammation and poor outcomes in hemodialysis patients. We hypothesized that patients with CVC, AVG, and AVF reported the highest, moderate, and lowest level of inflammatory markers, respectively, and patients with AVG and CVC have higher mortality than AVF
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