Detailing the Relation Between Renal T2* and Renal Tissue pO2 Using an Integrated Approach of Parametric Magnetic Resonance Imaging and Invasive Physiological Measurements

Objectives: This study was designed to detail the relation between renal T-2* and renal tissue pO(2) using an integrated approach that combines parametric magnetic resonance imaging (MRI) and quantitative physiological measurements (MR-PHYSIOL). Materials and Methods: Experiments were performed in 21 male Wistar rats. In vivo modulation of renal hemodynamics and oxygenation was achieved by brief periods of aortic occlusion, hypoxia, and hyperoxia. Renal perfusion pressure (RPP), renal blood flow (RBF), local cortical and medullary tissue pO(2), and blood flux were simultaneously recorded together with T-2*, T-2 mapping, and magnetic resonance-based kidney size measurements (MR-PHYSIOL). Magnetic resonance imaging was carried out on a 9.4-T small-animal magnetic resonance system. Relative changes in the invasive quantitative parameters were correlated with relative changes in the parameters derived from MRI using Spearman analysis and Pearson analysis. Results: Changes in T-2* qualitatively reflected tissue pO(2) changes induced by the interventions. T-2* versus pO(2) Spearman rank correlations were significant for all interventions, yet quantitative translation of T-2*/pO(2) correlations obtained for one intervention to another intervention proved not appropriate. The closest T-2*/pO(2) correlation was found for hypoxia and recovery. The interlayer comparison revealed closest T-2*/pO(2) correlations for the outer medulla and showed that extrapolation of results obtained for one renal layer to other renal layers must be made with due caution. For T-2* to RBF relation, significant Spearman correlations were deduced for all renal layers and for all interventions. T-2*/RBF correlations for the cortex and outer medulla were even superior to those between T-2* and tissue pO(2). The closest T-2*/RBF correlation occurred during hypoxia and recovery. Close correlations were observed between T(2)Z* and kidney size during hypoxia and recovery and for occlusion and recovery. In both cases, kidney size correlated well with renal vascular conductance, as did renal vascular conductance with T-2*. Our findings indicate that changes in T-2* qualitatively mirror changes in renal tissue pO(2) but are also associated with confounding factors including vascular volume fraction and tubular volume fraction. Conclusions: Our results demonstrate that MR-PHYSIOL is instrumental to detail the link between renal tissue pO(2) and T-2* in vivo. Unravelling the link between regional renal T-2* and tissue pO(2), including the role of the T-2* confounding parameters vascular and tubular volume fraction and oxy-hemoglobin dissociation curve, requires further research. These explorations are essential before the quantitative capabilities of parametric MRI can be translated from experimental research to improved clinical understanding of hemodynamics/oxygenation in kidney disorders.