Hemodialysis (HD) patients with double-lumen vascular access catheters (D-VAC) are at increased risk of bacteremia. Coinfection with hepatitis C virus (HCV) may be an additional risk factor for bacteremia in these patients. In this regard, we have shown that HCV-seropositive HD patients with D-VAC have an increased incidence of bacteremia when compared with patients seronegative for the virus (Sullivan et al. J Invest Med 2006;54:S289; Zaiden et al. JASN in press). On this basis, we theorized that the circulating HCV viral load may correlate with bacteremic events in these patients. To address this question, we reviewed the most recent records of the cohort from our previous work (in press). In this study, we surveyed for the presence of bacteremia during a 5-month period (5/06-10/06). In addition, we prospectively assessed the HCV viral load by measuring HCV RNA (RT-PCR) in all HCV-positive patients.
Results Ninety-nine patients were studied; mean age of 59 years, 38% male, and 64% African American. Twenty-one (21%) patients were HCV positive. For the 5-month study period, bacteremia data were available in 72 of 78 seronegative and 19 of 21 seropositive patients. The HCV-positive subjects demonstrated a numeric trend toward more frequent bacteremic events (5/19 [26%] vs 14/72 [19%] for HCV seropositive vs seronegative, respectively, p = .51). There was no difference in age of D-VAC between HCV-negative and -positive patients (mean ± SEM, 321 ± 20 vs 418 ± 41, respectively). Circulating viral titers were obtained in 18 of 21 HCV-positive patients. Eight of 18 (44%) had undetectable HCV levels, and 10 patients had measurable viral loads ((thousands) 778 ± 328 IU/mL). Sixteen patients with viral titers had bacteremia data available. In this group, there were no differences in viral titers between bacteremic and nonbacteremic patients (323 ± 458 vs 425 ± 264 IU/mL, respectively). In contrast, when patients with measurable titers (n = 8) were compared with patients with no detectable viral RNA (n = 8), there was a significant increase in bacteremic events (4/8 [50%] vs 0/8 respectively, p = .009, Chi-squared). These data support the contention that HCV infection may be a negative immunomodulator in HD patients with D-VAC and thus constitute a risk factor for infection from bacteremia.
Conclusion HD patients with D-VAC and HCV infection may be at increased risk of bacteremic events. These data suggest that the presence of detectable HCV RNA may be more important than the absolute circulating level of virus. Following HCV RNA expression in HD patients with D-VAC may allow for risk stratification for bacteremia and modulate the approach to management in these patients.
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