Search

Static intra-access pressure ratio (SIAPR) measurement, using haemodialysis machine transducers, is the vascular access surveillance method in patients undergoing haemodialysis. However, little is known about the relationship between the SIAPR and arterial stiffness, and the clinical usefulness of the SIAPR in predicting cardiovascular events. A total of 209 patients undergoing maintenance haemodialysis were evaluated. The SIAPRs ranged from 0.01 to 0.52 (median: 0.23). When the patients were divided into two groups according to their median of SIAPR, the incidence of previous cardiovascular disease, E/E′ ratio, and brachial-ankle pulse wave velocity were significantly higher in the patients with SIAPRs of ≤0.23 than in those with SIAPRs of >0.23. Conversely, patients with worse comorbid status had a lower SIAPR than patients without it. In the Kaplan-Meier analysis, the cumulative incidence of cardiovascular events was significantly higher in the patients with SIAPRs of ≤0.23 than in those with SIAPRs of >0.23 (P < 0.001). In the multiple Cox regression analysis, an increase in the SIAPR was associated with a reduced risk for cardiovascular events [hazard ratio: 0.36, 95% confidence interval: 0.21–0.60, P = 0.001]. Therefore, a low SIAPR related with arterial stiffness was a predictor for cardiovascular events. [ABSTRACT FROM AUTHOR]

Background: In hemodialysis patients, fluid overload and malnutrition are accompanied by extracellular fluid (ECF) expansion and intracellular fluid (ICF) depletion, respectively. We investigated the relationship between ECF/ICF ratio (as an integrated marker reflecting both fluid overload and malnutrition) and survival and cardiovascular disease (CVD) in the context of malnutrition-inflammation-arteriosclerosis (MIA) complex. Methods: Seventy-seven patients from a single hemodialysis unit were prospectively enrolled. The ECF/ICF volume was measured by segmental multi-frequency bioimpedance analysis. MIA and volume status were measured by serum albumin, C-reactive protein (CRP), pulse wave velocity (PWV) and plasma B-type natriuretic peptide (BNP), respectively. Results: The mean ECF/ICF ratio was 0.56±0.06 and the cut-off value for maximum discrimination of survival was 0.57. Compared with the low ECF/ICF group, the high ECF/ICF group (ratio≥0.57, 42%) had higher all-cause mortality, CVD, CRP, PWV, and BNP, but lower serum albumin. During the 5-year follow-up, 24 all-cause mortality and 38 CVD occurred (18 and 24, respectively, in the high ECF/ICF group versus 6 and 14 respectively in the low ECF/ICF group, P<0.001). In the adjusted Cox analysis, the ECF/ICF ratio nullifies the effects of the MIA and volume status on survival and CVD and was an independent predictor of all-cause mortality and CVD: hazard ratio (95% confidence interval); 1.12 (1.01–1.25) and 1.09 (1.01–1.18) for a 0.01 increase in the ECF/ICF ratio. The degree of malnutrition (albumin), inflammation (CRP), arteriosclerosis (PWV), and fluid overload (BNP) were correlated well with the ECF/ICF ratio. Conclusions: Hemodialysis patients with high ECF/ICF ratio are not only fluid overloaded, but malnourished and have stiff artery with more inflammation. The ECF/ICF ratio is highly related to the MIA complex, and is a major risk indicator for all-cause mortality and CVD. [ABSTRACT FROM AUTHOR]

Background: In chronic hemodialysis patients, malnutrition, inflammation, depression and arteriosclerosis are pathogenetically associated suggesting the presence of malnutrition-inflammation-depression-arteriosclerosis (MIDA) complex acting as a risk factor for cardiovascular disease (CVD). Methods: Nutritional status was assessed by serum albumin, subjective global assessment and normalized protein catabolic rate (nPCR). Inflammation was assessed by serum high-sensitivity C-reactive protein (hsCRP). Depression was assessed with the Beck Depression Inventory and DSM-IV criteria. The severity of arteriosclerosis was measured by pulse wave velocity (PWV). Results: Among 81 hemodialysis patients, 44 (54.3%) had malnutrition (albumin <4.0 mg/dl with subjective global assessment score <6 and/or nPCR <1.0) and 39 (48.1%) had inflammation (hsCRP >1 mg/l). The prevalence of depression was 50.6% (n = 41). Fifty-nine (73.8%) had arteriosclerosis (measured PWV > expected PWV based on age/blood pressure/gender adjustment). The severity of the all four individual MIDA components correlated well with each other. The average number of the MIDA complication (MIDA score) was 2.27 ± 1.33. -During the 5-year follow-up, 40 cases of CVD and 26 cases of all-cause death occurred. In Cox analysis adjusted for -previous CVD, age, diabetes, blood pressure, pulse pressure, intradialytic hypotension, B-type natriuretic peptide, -hemoglobin and hemodialysis incompliance, the MIDA score was an independent predictor of CVD and all-cause death: hazard ratio (95% confidence interval); 1.89 (1.13-3.17) and 3.48 (1.32-9.21) for an increase of 1 MIDA score. Conclusions: This study suggests the presence of MIDA complex, which is composed of malnutrition, inflammation, depression and arteriosclerosis. The MIDA complex syndrome was an independent risk factor for CVD and all-cause death in chronic hemodialysis patients. Copyright © 2013 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Background: Sarcopenia involves an age-related decline in skeletal muscle mass with functional disability or low muscle strength. Vascular calcification (VC) occurs commonly in patients with chronic kidney disease, in whom it is associated with cardiovascular disease. We aimed to investigate the correlations of low muscle mass with the quantified vascular calcification score (VCS) of the arm of vascular access, as well as whether low muscle mass is associated with the incidence of vascular access failure. Methods: The VCS was measured on non-contrast, arm computed tomography using the Agatston method. The lower muscle mass (LMM) group comprised subjects whose skeletal muscle mass of the lower extremities, as measured using bioelectrical impedance, was lower than the median. Higher VC was defined as a score of 500 or above, corresponding to the highest 40% of VCS. The relationship between LMM and VC was explored using univariate and multivariate logistic regression analyses. Results: Seventy-five patients were included, of whom forty-two (56.0%) were men. The median age was 64 years (interquartile range 58–72 years). Of the 75 patients, 73 satisfied the diagnostic criteria for sarcopenia. The median hemodialysis vintage was 49.4 months (range 32.1–99.2 months). No significant differences were found between the non-LMM and LMM groups in sex, end-stage renal disease etiology, and type of vascular access, although the LMM group showed significantly older age and hemodialysis vintage. LMM presented a significant association with VC (hazard ratio (HR) 3.562; 95% CI, 1.341–9.463; p = 0.011). Upon adjustment for hemodialysis vintage, diabetes, and systolic blood pressure, LMM demonstrated an independent association with VC (HR, 10.415; 95% CI, 2.357–46.024; p = 0.002). The risk of vascular access failure was higher in the LMM group (HR, 3.652; 95%, CI 1.135–11.749; p = 0.03). VC was a full mediator in the relationship of LMM with recurrent vascular access failure. Conclusions: We quantified LMM via bioimpedance analysis and found a heretofore-unreported association between LMM and vascular access failure. LMM increases the risk of VC and has the potential to predict vascular access failure. [ABSTRACT FROM AUTHOR]