Toward a full-scale model of renal hemodynamics using a reconstructed vascular tree.

IF 3.4 American journal of physiology. Renal physiology Pub Date : 2025-05-01 Epub Date: 2025-03-18 DOI:10.1152/ajprenal.00293.2024
Peidi Xu, Sune Darkner, Olga Sosnovtseva, Niels-Henrik Holstein-Rathlou
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Abstract

The kidney's vascular network stands out because 1) the microcirculation not only supplies the tissues with oxygen and nutrients but also supports glomerular filtration in each nephron, 2) it contains the tubuloglomerular feedback, a mechanism that contributes to renal blood flow autoregulation and is unique to the kidney, and 3) the topology of the renal arterial network influences signaling along the vessels mediating nephron-nephron interactions. We have developed a full-scale vascular model of the rat kidney based on a reconstructed vascular network combined with a nephron model that includes glomerular filtration, tubular reabsorption, and autoregulation of afferent arteriolar resistances. The model evaluates the steady-state operating conditions of approximately 30,000 nephrons in a rat kidney and the efficiency of autoregulation under normal and pathological conditions. The simulation results show how the regulated afferent arteriolar resistances stabilize blood flow in the reconstructed full-scale renal vascular network. It is concluded that by using a reconstructed renal vascular tree, it is possible to develop a realistic full-scale model of the regulation of renal hemodynamics as a first step toward creating a virtual kidney.NEW & NOTEWORTHY We have developed the first full-scale steady-state model integrating a realistic vascular network topology of the kidney and its hemodynamic regulatory mechanisms. The vascular network is combined with approximately 30,000 nephron models that include glomerular filtration, tubular reabsorption, and autoregulation of the afferent arteriolar resistances. By simulating the adaptive properties of the renal microcirculation at steady state, our approach demonstrates the feasibility of utilizing a reconstructed vascular network for comprehensive modeling of renal function.

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利用重建血管树建立全尺寸肾脏血流动力学模型。
肾脏的血管网络之所以突出,是因为(i)微循环不仅为组织提供氧气和营养,而且还支持每个肾元的肾小球滤过,(ii)包含小管肾小球反馈,这是一种有助于肾血流自动调节的机制,是肾脏所独有的,(iii)肾动脉网络的拓扑结构影响着介导肾元-肾元相互作用的血管信号传导。我们建立了大鼠肾脏的全尺寸血管模型,该模型基于重建的血管网络和肾元模型,包括肾小球滤过、肾小管重吸收和传入小动脉阻力的自动调节。该模型评估了大鼠肾脏中约30,000个肾单位的稳态工作条件以及正常和病理条件下的自动调节效率。模拟结果显示了传入小动脉阻力的调节是如何稳定重建的全尺寸肾血管网络中的血流的。结论是,通过重建肾脏血管树,有可能开发一个真实的肾脏血流动力学调节全尺寸模型,作为创建虚拟肾脏的第一步。
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Correction for Trott et al., volume 315, 2018, p. F1855-F1868. Correction for Hamatani et al., volume 330, 2026, p. F269-F284. The transcription factor Tcf21 is necessary for adoption of cell fates by Foxd1+ stromal progenitors during kidney development. Making a portal for podocyte-parietal cell communication in glomerular injury. Kidney kallikrein-1 contributes to cleavage of γ-ENaC in vivo.
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