ASSESSMENT OF STIFFNESS OF LARGE TO SMALL ARTERIES IN MULTI-STAGE RENAL DISEASE: A NUMERICAL STUDY

Abstract

Objective: Arterial stiffness, as assessed via pulse wave velocity (PWV), is a major biomarker for risk assessment in patients with chronic kidney disease. However, the mechanisms responsible for the changes in PWV in the presence of kidney disease are not yet fully elucidated. In the present study, we aimed to investigate the direct effects attributable to biomechanical alterations to the arterial tree caused by renal disease progression on arterial stiffness, independent of any biochemical or compensatory effects. Design and method: Particularly, we used a previously validated one-dimensional (1-D) model of the cardiovascular system to simulate arterial pressure and flow at control with two kidneys (2KDN) and in arterial tree configurations representative of different stages of kidney disease, namely subject with a single functional kidney (1KDN), without any functional kidney (0KDN) and a transplant recipient (TX) with a single functional kidney re-attached to the external iliac artery. We evaluated the respective variations in blood pressure (BP), as well as arterial stiffness of large, medium, and small-sized vessels via carotid-femoral PWV (cfPWV), carotid-radial PWV (crPWV), and radial-digital PWV (rdPWV), respectively. Results: Our results showed that BP was increased in 1KDN and 0KDN, and that systolic BP values were restored in the TX configuration. Furthermore, a rise was reported in all PWVs for all tested configurations. The relative difference in stiffness from control to 0KDN was higher in the case of crPWV (+20 %); approximately twice the difference observed for cfPWV and rdPWV (+11 %). In TX, we observed a restoration of the PWVs to values close to 1KDN. Globally, it was demonstrated that alterations of the outflow boundaries to the renal arteries as occurring in different stages of renal disease lead to changes in blood pressure and central and peripheral PWV in line with previously reported clinical data. Conclusions: Our findings suggest that the PWV variations observed in clinical practice with renal disease progression may be partially attributed to biomechanical alterations of the arterial tree, and their effect on blood pressure.