Blood flow into the kidneys through the renal artery determines the systemic blood pressure which is regulated by the baroreceptors in the kidneys. When the baroreceptors sense decreases in local fluid pressure they stimulate the renin-angiotensin aldosterone (RAA) system, which increases systemic blood pressure by constricting blood vessels throughout the body.

An aneurysm in the renal artery leads to high systemic blood pressure in most patients with this condition, but the mechanisms by which the pressure increase occurs are not well understood. One explanation of the pressure increase could be a drop in local fluid pressure near the aneurysm itself causing the RAA system to “correct” this low pressure by systemically increasing the blood pressure.

The ongoing work reported here has focused on a model renal artery network with and without an aneurysm by simulating the flow with computational fluid dynamics (CFD) software. The fluid for the simulations was meant to mimic blood in terms of density and viscosity for shear stresses where Non-Newtonian flow effects should not be a concern. Flow into the renal artery was at a Reynolds number of almost 700, to mimic the flow rate in the renal artery. The simulations were performed to determine the difference in pressure between an inlet to the renal network and the exits from the network. These results indicate that the pressure difference through the network differed by less than 10 Pa comparing networks with and without saccular aneurysm. The pressure change that would trigger the RAA system is nearly 1000 Pa. So we conclude that the effect of changing the geometry with only a saccular aneurysm is not responsible for triggering the RAA system alone. Other effects that could lead to triggering of the RAA system are discussed as well as our initial construction of a system to perform validation experiments of our CFD results.

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