Abstract
Renal tissue hypoperfusion and hypoxia are early key elements in the pathophysiology of acute kidney injury of various origins, and may also promote progression from acute injury to chronic kidney disease. Here we describe basic principles of methodology to quantify renal hemodynamics and tissue oxygenation by means of invasive probes in experimental animals. Advantages and disadvantages of the various methods are discussed in the context of the heterogeneity of renal tissue perfusion and oxygenation.This chapter is based upon work from the COST Action PARENCHIMA, a community-driven network funded by the European Cooperation in Science and Technology (COST) program of the European Union, which aims to improve the reproducibility and standardization of renal MRI biomarkers. This introduction chapter is complemented by a separate chapter describing the experimental procedure and data analysis.
Highlights
Animal studies have provided evidence that acute kidney injury (AKI) of various origins shares a common link in the pathophysiological chain of events, leading to AKI, as well as to progression from AKI to chronic kidney disease (CKD): imbalance between renal oxygen delivery and oxygen demand [3, 6–13]
Renal tissue hypoperfusion and hypoxia have been suggested to play a pivotal role in the pathophysiology of other kidney diseases including diabetic kidney disease [14–16]
These methods have been used (1) to study mechanisms of physiological control of renal hemodynamics and oxygenation and (2) the effects of various substances on this control in healthy animals, (3) to test several putative preventive or therapeutic approaches for AKI and CKD in animal models, and (4) for the purpose of calibrating functional magnetic resonance imaging (MRI) including renal blood oxygenation level-dependent MRI (BOLD-MRI) that makes use of the quantitative MR parameter T2*, which is a surrogate for blood oxygenation [18–28]
Summary
Kidney diseases are a global health burden with steadily increasing prevalence and incidence [1–5]. These measurements reveal that local tissue pO2 levels in the cortex vary dramatically, foremost according to the distance to the “vascular bundles” of interlobular arteries and veins: pO2 values range from 10 mmHg at the greatest distance from two neighboring “bundles,” to up to 70 mmHg around the “bundles.” In addition, local cortical tissue pO2 varies with the distance to the arcuate arteries located at the corticomedullary boundary. The high O2 demands of the thick ascending limbs in relation to the rather low O2 supply of the outer medulla, consequent to its particular vascular architecture, exposes this renal layer to the greatest risk for hypoxic tissue damage [6–14, 43, 51, 52]
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