Proceedings on Automation in Medical Engineering
Vol. 3 No. 1 (2026): Proc AUTOMED
https://doi.org/10.18416/AUTOMED.2026.2536

18th Interdisciplinary AUTOMED Symposium in Collaboration with the TC Medical Robotics, 2536

Object-oriented Modeling of Renal Autoregulation for a Cardiovascular System

Main Article Content

Markus Lueken (Medical Information Technology, RWTH Aachen University), Steffen Leonhardt (Medical Information Technology, RWTH Aachen University), Marian Walter (Medical Information Technology, RWTH Aachen University)

Abstract

Renal autoregulation maintains blood flow over a wide range of perfusion pressures despite pronounced nonlinear vessel mechanics and neurogenic influences. In lumped-parameter cardiovascular models, vascular beds are commonly represented by linear resistive elements, which are insufficient to reproduce characteristic pressure–flow relationships, critical closing pressure, and dynamic myogenic responses.


In this work, a nonlinear representation of the renal vascular resistance is proposed based on an extended MOSFET-inspired circuit analogy. The model allows pressure-dependent conductance, flow limitation at low pressures, and systematic shifts of the pressure–flow characteristic under varying sympathetic activation. This approach enables a compact yet expressive description of arteriolar behavior within an electrical equivalent circuit framework.


To emulate renal autoregulation, a phenomenological control concept is introduced that combines two complementary mechanisms acting on different time scales. A fast pressure-driven component represents the myogenic response to changes in perfusion pressure, while a slow adaptive component integrates flow error and aggregates the net effect of metabolic, renal, and humoral regulation. Physiological actuator dynamics are enforced using first-order dynamics, rate limiting, and saturation with anti-windup protection.


Simulation results demonstrate that the proposed model reproduces key features of renal autoregulation, including a transient flow overshoot following pressure perturbations, subsequent active flow reduction, and restoration of renal blood flow toward a reference level over time. Static pressure–flow characteristics further exhibit an extended autoregulatory plateau and a pressure-dependent critical closing pressure.


The presented approach provides a computationally efficient and physiologically interpretable extension of lumped-parameter cardiovascular models and is well suited for system-level simulations of renal hemodynamics.

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