Dendritic Cell Dysfunction in Patients with End-stage Renal Disease.

End-stage renal disease (ESRD) with immune disorder involves complex interactions between the innate and adaptive immune responses. ESRD is associated with various alterations in immune function such as a reduction in polymorphonuclear leukocyte bactericidal activity, a suppression of lymphocyte proliferative response to stimuli, and a malfunction of cell-mediated immunity at the molecular level. ESRD also increases patients' propensity for infections and malignancies as well as causing a diminished response to vaccination. Several factors influence the immunodeficiency in patients with ESRD, including uremic toxins, malnutrition, chronic inflammation, and the therapeutic dialysis modality. The alteration of T-cell function in ESRD has been considered to be a major factor underlying the impaired adaptive cellular immunity in these patients. However, cumulative evidence has suggested that the immune defect in ESRD can be caused by an Ag-presenting dendritic cell (DC) dysfunction in addition to a T-cell defect. It has been reported that ESRD has a deleterious effect on DCs both in terms of their number and function, although the precise mechanism by which DC function becomes altered in these patients is unclear. In this review, we discuss the effects of ESRD on the number and function of DCs and propose a possible molecular mechanism for DC dysfunction. We also address therapeutic approaches to improve immune function by optimally activating DCs in patients with ESRD.

Effectiveness of beraprost sodium in maintaining vascular access patency in patients on hemodialysis.

PURPOSE: Hemodialysis vascular access dysfunction, mostly attributed to neointimal hyperplasia, is a major cause of morbidity and hospitalization in patients on hemodialysis. It has been reported that prostaglandin I2 has pleiotropic effects including anti-platelet, vasodilating, anti-inflammatory, and anti-atherogenic properties. In addition, several studies have shown that prostaglandin I2 can inhibit neointimal formation after vascular injury. This study aimed to investigate the effects of beraprost sodium, an oral synthetic analog of prostaglandin I2, on vascular access patency in patients on hemodialysis who experienced primary hemodialysis vascular access failure. METHODS: Fifty-five patients with end-stage renal disease who were on hemodialysis were prospectively selected for this study. Twenty-three patients were assigned to be treated with 120 µg/day of beraprost sodium, while remaining patients (n = 32) were assigned to a control group. The primary outcome was primary unassisted vascular access patency at 2 years. RESULTS: The incidence of primary unassisted patency at 2 years was 83% in the beraprost sodium group and 38% in the control group (p = 0.001). Analysis of covariables indicated that this effect occurred mainly as a result of beraprost sodium administration. No life-threatening adverse event or severe bleeding was recorded in any of the groups. CONCLUSIONS: Our data indicated that an oral prostaglandin I2 analog, beraprost sodium, is effective and safe for the maintenance of vascular access patency in patients on hemodialysis with primary vascular access failure.

Surgical removal of endovascular stent after migration to the right ventricle following right subclavian vein deployment for treatment of central venous stenosis.

Central venous stenosis or occlusion occurs in 11-50% of hemodialysis patients with prior subclavian vein cannulation and ipsilateral fistula or shunt. Most patients are asymptomatic but some require treatment to reduce the risk of thrombosis and improve inadequate hemodialysis pressure. In these cases, endovascular intervention, including ballooning and stenting, is a feasible strategy for selected patents. We report an unusual case of a 40-year-old man on hemodialysis that underwent endovascular stenting to treat right subclavian vein stenosis and experienced stent migration to the right ventricle, requiring surgical removal.