Concentrations of N-terminal pro brain natriuretic peptide (NT-proBNP) increase in patients with heart failure and other cardiovascular (CV) diseases and are strong prognostic markers. In patients with end-stage renal disease (ESRD) in hemodialysis (HD), levels of NT-proBNP are almost always raised. In ESRD patients undergoing HD, we aimed at (i) identifying the factors that affect levels of NT-proBNP, (ii) determining the effect of HD on NT-proBNP, and (iii) determining the prognostic impact of NT-proBNP. A total of 109 patients underwent physical examination, electrocardiogram, and echocardiography. Serum NT-proBNP was measured before and after HD (Elecsys 2010). NT-proBNP levels were markedly elevated (pre-HD 4079 pg/ml, post-HD 2759 pg/ml, P<0.001). There was a strong inverse correlation between NT-proBNP and left ventricular ejection fraction (LVEF) (P=0.043), 24-h urine production (P=0.006), and K(t)/V (efficacy of dialysis) (P=0.016) and a positive correlation with left ventricular hypertrophy (LVH) (P=0.014). Patients with higher concentrations, both pre- and post-HD had an increased mortality rate compared to those with lower concentrations (P=0.007, P=0.002). We found age (P=0.009) and NT-proBNP (pre-HD P=0.007, post-HD P=0.001) predictive of death. Our findings demonstrate that CV disease in terms of LVH and reduced LVEF in addition to 24-h urine production and K(t)/V determine NT-proBNP levels. Post-HD levels of NT-proBNP were lower than pre-HD levels; both predictive of mortality.

Intradialytic hypotension (IDH) is one of the most important short-term complications to hemodialysis (HD). Inadequate cardiac filling due to a reduction in the central blood volume is believed to be a major etiological factor. The aim of this study was to evaluate whether these pathophysiologic events are reflected in the central venous oxygen saturation (ScO(2)) and thoracic admittance (TA) during dialysis. Twenty ambulatory HD patients, 11 hypotension prone (HP) and 9 hypotension resistant, with central vascular access, were monitored during 3 HD sessions each. ScO(2), TA, finger blood pressure (BP), and relative change in blood volume (DeltaBV) were measured and sampled continuously. The relative TA decrease and DeltaBV were both largest in the HP group (p<0.05 for both), whereas ScO(2) decreased only in HP patients (p<0.001). Baseline TA was lower in the HP group (p<0.01). Changes in ScO(2) and TA correlated much closer than did changes in ScO(2) and DeltaBV (r=0.43 and 0.18, respectively). Our results suggest that an intradialytic decrease in cardiac output, as reflected by a fall in ScO(2), is a common feature to HD patients prone to IDH. In patients using a central vascular access, ScO(2) and TA measurements may be more specific to the pathophysiologic events preceding IDH than DeltaBV-the current standard monitoring method.

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Reliable methods for cardiac output determination are essential for studying the pathophysiology of intradialytic hypotension. Use of the current gold standard, the Transonic monitor, requires an arteriovenous fistula. We wished to verify the accuracy of a method based on finger pulse contour analysis, namely the Finometer monitor (FNM) for further use on patients dialyzing on a central vascular catheter. Fifty simultaneous cardiac output measurements were obtained during hemodialysis sessions in 25 patients. The internal variability of the FNM measurements was assessed by comparing 24 pairs of immediately successive measurements. The variability of successive FNM measurements was small (bias 0.28%, SD +/- 6.1%; NS). The absolute cardiac output values reported by the FNM were unreliable (bias 20.1%, SD +/- 35.3%; P<0.001) as were the relative intradialytic changes (r(2)=0.01). Excluding participants from the analysis due to old age, high dialysis vintage or a suspicion of atherosclerosis did not improve the results. Our findings do not support the use of pulse contour analysis for measuring cardiac output in hemodialysis patients. Uremic vascular disease may be the cause of the observed inaccuracy.

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