ABSTRACT
Vascular access intervention therapy (VAIVT) has been positioned as the first choice of treatment for stenosis lesions frequently observed in arteriovenous fistula (AVF) for hemodialysis patients in Japan. Furthermore, increased blood flow can provide a stable dialysis. In contrast, it has been reported that excess blood flow of AVF causes high-output heart failure. Although VAIVT is used to increase blood flow of AVF, the impact of VAIVT on cardiac load has been rarely reported. We examined the factors associated with cardiac load in hemodialysis patients undergoing VAIVT by measuring levels of α human atrial natriuretic polypeptide (hANP) and brain natriuretic peptide (BNP) before and after VAIVT. Data were extracted on hemodialysis patients who underwent measurements of αhANP and BNP in before and after VAIVT at our facility and related facilities between February 2014 and December 2014. Nineteeen patients (median age, 73.0 [66.5-80.5] years; male, 52.6%; 36.8% with diabetes; median duration of dialysis treatment, 50.0 [21-109] months) were enrolled in this study. Flow volume of AVF was higher after VAIVT than that before VAIVT (442.0 vs. 758.0 mL/minute, P < 0.001). Moreover, resistance index (RI) of AVF after VAIVT was lower than that before VAIVT (0.61 vs. 0.53, P < 0.01). Although αhANP did not change before and after VAIVT (55.6 vs. 54.9 pg/mL, P = 0.099), BNP after VAIVT was significantly higher than that before VAIVT (145.2 vs. 175.0 pg/mL, P < 0.05). Factors correlated with the increase in BNP were flow volume of AVF before VAIVT (r = -0.458, P = 0.049) and levels of BNP before VAIVT (r = 0.472, P = 0.041). There was no significant correlation between the increase in αhANP with flow volume of AVF before VAIVT, levels of αhANP before VAIVT. Patients with high levels of BNP and low flow volume of AVF before VAIVT were considered to have a high risk of developing heart failure after VAIVT.
ABSTRACT
Oxidative stress may contribute to the pathogenesis of diabetic nephropathy (DN), although the detailed mechanism of reactive oxygen species (ROS) regulation is still unclear. This study examined the effect of high-salt diet on ROS production and expression of antioxidant enzymes in control and experimentally diabetic rats. Wistar fatty rats (WFR) as a type 2 diabetes mellitus model and Wistar lean rats (WLR) as a control were fed a normal-salt diet (NS) and high-salt diet (HS) from the age of 6 to 14 weeks. We then examined the blood pressure, urinary albumin excretion (UAE), and urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG) levels. The expression of antioxidant enzymes including alpha-catalase (CAT), Cu-Zn superoxide dismutase (SOD), Mn SOD, and glutathione peroxidase (GPx) were analyzed in the glomeruli of the rats using Western blotting. The expression of NAD(P)H oxidase p47(phox) and NFkappaB p65 was evaluated using immunohistochemical staining. By 14 weeks of age, the WFR-HS group exhibited hypertension and markedly increased UAE. The level of 8-OHdG, a marker of oxidative damage, in the WFR-HS group was also higher than that in the WLR groups or WFR-NS group. The expression of alpha-CAT and Mn SOD proteins was significantly decreased in isolated glomeruli in the WFR-HS group. GPx and Cu-Zn SOD expression did not differ between the WFR and WLR groups. High expression of ROS and decreases in antioxidants were seen in the glomeruli of diabetic rats with hypertension, suggesting that oxidative stress may be involved in the development of DN.
