Membrane bioincompatibility was demonstrated by successive white blood cell counts and C3a generation. Pulse wave analysis was obtained by applanation tonometry (SphygmoCor) in a sequential way: basal, after 30 minutes with nul ultrafiltration, and after a complete dialysis with ultrafiltration. At 15 minutes of haemodialysis, significant decrease in leukocyte count occurred: versus ( ), while C3a levels sharply increased from to ？ng/mL ( ). No changes were observed in augmentation index without ultrafiltration: versus . Only aortic systolic blood pressure was lower at 15 minutes: versus ？mmHg ( ), in agreement with a reduction in brachial systolic blood pressure: versus ？mmHg ( ), without changes in aortic or brachial diastolic blood pressure. Important changes in pulse wave analysis were observed after a complete haemodialysis session: augmentation index versus , aortic systolic blood pressure versus mmHg ( ), without changes in aortic diastolic blood pressure. In summary, haemodialysis with cellulose diacetate acutely induced a transient state of immunoactivation due to bioincompatibility, this phenomenon was nondetectable by pulse wave analysis. Complete haemodialysis session led to important changes in pulse wave analysis. 1. Introduction Cardiovascular (CV) disease is the main cause of morbidity and mortality in patients with end-stage renal disease (ESRD). The increased risk is partly due to a higher prevalence of traditional CV risk factors. Nevertheless, these patients also present other nontraditional CV risk factors related with the setting of uremic background [1] that result in functional and structural alterations of the arterial wall, leading to an increase in arterial stiffness. As in the general population, arterial stiffening has been described as an independent predictor of both CV and overall mortality in haemodialysis (HD) patients [2–8]. Another component that has been proposed to play a role in CV risk is the HD session per se. The dialysis procedure may induce acute functional alterations of the arterial wall through several mechanisms, the most remarkable being the intermittent immunoactivation state induced by dialysis [9–11], and the acute intravascular volume drop produced during the HD session [12–17]. It has been proposed that these acute functional alterations could be detected by noninvasive pulse wave analysis (PWA) [12]. As PWA measurements are being increasingly introduced in the clinical setting, the main objective of our study was to separately analyze the acute effects on PWA of bioincompatibility and
References
[1]
R. N. Foley, P. S. Parfrey, and M. J. Sarnak, “Clinical epidemiology of cardiovascular disease in chronic renal disease,” American Journal of Kidney Diseases, vol. 32, no. 5, supplement 3, pp. S112–S119, 1998.
[2]
G. M. London, S. J. Marchais, A. P. Guerin, F. Metivier, and H. Adda, “Arterial structure and function in end-stage renal disease,” Nephrology Dialysis Transplantation, vol. 17, no. 10, pp. 1713–1724, 2002.
[3]
A. Covic, P. Gusbeth-Tatomir, and D. J. A. Goldsmith, “Arterial stiffness in renal patients: an update,” American Journal of Kidney Diseases, vol. 45, no. 6, pp. 965–977, 2005.
[4]
G. M. London, J. Blacher, B. Pannier, A. P. Guérin, S. J. Marchais, and M. E. Safar, “Arterial wave reflections and survival in end-stage renal failure,” Hypertension, vol. 38, no. 3, pp. 434–438, 2001.
[5]
J. Blacher, A. P. Guerin, B. Pannier, S. J. Marchais, M. E. Safar, and G. M. London, “Impact of aortic stiffness on survival in end-stage renal disease,” Circulation, vol. 99, no. 18, pp. 2434–2439, 1999.
[6]
J. Blacher, M. E. Safar, A. P. Guerin, B. Pannier, S. J. Marchais, and G. M. London, “Aortic pulse wave velocity index and mortality in end-stage renal disease,” Kidney International, vol. 63, no. 5, pp. 1852–1860, 2003.
[7]
M. E. Safar, J. Blacher, B. Pannier et al., “Central pulse pressure and mortality in end-stage renal disease,” Hypertension, vol. 39, no. 3, pp. 735–738, 2002.
[8]
J. Blacher, M. E. Safar, B. Pannier, A. P. Guerin, S. J. Marchais, and G. M. London, “Prognostic significance of arterial stiffness measurements in end-stage renal disease patients,” Current Opinion in Nephrology and Hypertension, vol. 11, no. 6, pp. 629–634, 2002.
[9]
A. Mourad, S. Carney, A. Gillies, B. Jones, R. Nanra, and P. Trevillian, “Acute effect of haemodialysis on arterial stiffness: membrane bioincompatibility?” Nephrology Dialysis Transplantation, vol. 19, no. 11, pp. 2797–2802, 2004.
[10]
M. Kosch, A. Lever, M. Fobker et al., “Dialysis filter type determines the acute of haemodialysis on endothelial function and oxidative stress,” Nephrology Dialysis Transplantation, vol. 18, no. 7, pp. 1370–1375, 2003.
[11]
J. C. Korevaar, J. G. Van Manen, F. W. Dekker, D. R. De Waart, E. W. Boeschoten, and R. T. Krediet, “Effect of an increase in C-reactive protein level during a hemodialysis session on mortality,” Journal of the American Society of Nephrology, vol. 15, no. 11, pp. 2916–2922, 2004.
[12]
A. Covic, D. J. A. Goldsmith, L. Panaghiu, M. Covic, and J. Sedor, “Analysis of the effect of hemodialysis on peripheral and central arterial pressure waveforms,” Kidney International, vol. 57, no. 6, pp. 2634–2643, 2000.
[13]
J. L. Tycho Vuurmans, W. H. Boer, W. J. W. Bos, P. J. Blankestijn, and H. A. Koomans, “Contribution of volume overload and angiotensin II to the increased pulse wave velocity of hemodialysis patients,” Journal of the American Society of Nephrology, vol. 13, no. 1, pp. 177–183, 2002.
[14]
E. H. Y. Ie, T. L. M. De Backer, S. G. Carlier et al., “Ultrafiltration improves aortic compliance in haemodialysis patients,” Journal of Human Hypertension, vol. 19, no. 6, pp. 439–444, 2005.
[15]
B. Di Iorio, P. Nazzaro, E. Cucciniello, and V. Bellizzi, “Influence of haemodialysis on variability of pulse wave velocity in chronic haemodialysis patients,” Nephrology Dialysis Transplantation, vol. 25, no. 5, pp. 1579–1583, 2010.
[16]
S. Aure, E. Gersbach, M. Kandarpa, et al., “Effect of ultrafiltration on aortic augmentation pressure and index in patients on maintenance hemodialysis (abstract),” American Journal of Kidney Diseases, vol. 51, no. 4, p. B33, 2008.
[17]
N. G. Mardare, D. J. A. Goldsmith, P. Gusbeth-Tatomir, and A. Covic, “Intradialytic changes in reflective properties of the arterial system during a single hemodialysis session,” Hemodialysis International, vol. 9, no. 4, pp. 376–382, 2005.
[18]
M. Barenbrock, C. Spieker, V. Laske et al., “Studies of the vessel wall properties in hemodialysis patients,” Kidney International, vol. 45, no. 5, pp. 1397–1400, 1994.
[19]
A. Covic, D. J. A. Goldsmith, P. Gusbeth-Tatomir, and M. Covic, “Haemodialysis acutely improves endothelium-independent vasomotor function without significantly influencing the endothelium-mediated abnormal response to a β2-agonist,” Nephrology Dialysis Transplantation, vol. 19, no. 3, pp. 637–643, 2004.
[20]
A. Covic, N. Mardare, P. Gusbeth-Tatomir et al., “Increased arterial stiffness in children on haemodialysis,” Nephrology Dialysis Transplantation, vol. 21, no. 3, pp. 729–735, 2006.
[21]
Y. P. Lin, W. C. Yu, and C. H. Chen, “Acute versus chronic volume overload on arterial stiffness in haemodialysis patients,” Journal of Human Hypertension, vol. 19, no. 6, pp. 425–427, 2005.
[22]
M. Kosch, A. Levers, M. Barenbrock et al., “Acute effects of haemodialysis on endothelial function and large artery elasticity,” Nephrology Dialysis Transplantation, vol. 16, no. 8, pp. 1663–1668, 2001.
[23]
J. Kyriazis, I. Katsipi, K. Stylianou, N. Jenakis, A. Karida, and E. Daphnis, “Arterial stiffness alterations during hemodialysis: the role of dialysate calcium,” Nephron, vol. 106, no. 1, pp. c34–c42, 2007.
[24]
S. Marchais, A. Guerin, M. Safar, and G. London, “Arterial compliance in uraemia,” Journal of Hypertension, vol. 7, no. 6, pp. S84–S85, 1989.
[25]
P. K. Li, Y. L. Cheng, C. B. Leung, et al., “Effect of membrane permeability on inflammation and arterial stiffness: a randomized trial,” Clinical Journal of the American Society of Nephrology, vol. 5, pp. 652–658, 2010.
[26]
I. Soveri, L. Lind, B. Wikstr？m, M. Zilmer, K. Zilmer, and B. Fellstr？m, “Improvement in central arterial pressure waveform during hemodialysis is related to a reduction in asymmetric dimethylarginine (ADMA) levels,” Nephron, vol. 106, no. 4, pp. c180–c186, 2007.
