Abstract
Background: This paper outlines a multiparametric renal MRI acquisition and analysis protocol to allow non-invasive assessment of hemodynamics (renal artery blood flow and perfusion), oxygenation (BOLD T2*), and microstructure (diffusion, T1 mapping).Methods: We use our multiparametric renal MRI protocol to provide (1) a comprehensive set of MRI parameters [renal artery and vein blood flow, perfusion, T1, T2*, diffusion (ADC, D, D*, fp), and total kidney volume] in a large cohort of healthy participants (127 participants with mean age of 41 ± 19 years) and show the MR field strength (1.5 T vs. 3 T) dependence of T1 and T2* relaxation times; (2) the repeatability of multiparametric MRI measures in 11 healthy participants; (3) changes in MRI measures in response to hypercapnic and hyperoxic modulations in six healthy participants; and (4) pilot data showing the application of the multiparametric protocol in 11 patients with Chronic Kidney Disease (CKD).Results: Baseline measures were in-line with literature values, and as expected, T1-values were longer at 3 T compared with 1.5 T, with increased T1 corticomedullary differentiation at 3 T. Conversely, T2* was longer at 1.5 T. Inter-scan coefficients of variation (CoVs) of T1 mapping and ADC were very good at <2.9%. Intra class correlations (ICCs) were high for cortex perfusion (0.801), cortex and medulla T1 (0.848 and 0.997 using SE-EPI), and renal artery flow (0.844). In response to hypercapnia, a decrease in cortex T2* was observed, whilst no significant effect of hyperoxia on T2* was found. In CKD patients, renal artery and vein blood flow, and renal perfusion was lower than for healthy participants. Renal cortex and medulla T1 was significantly higher in CKD patients compared to healthy participants, with corticomedullary T1 differentiation reduced in CKD patients compared to healthy participants. No significant difference was found in renal T2*.Conclusions: Multiparametric MRI is a powerful technique for the assessment of changes in structure, hemodynamics, and oxygenation in a single scan session. This protocol provides the potential to assess the pathophysiological mechanisms in various etiologies of renal disease, and to assess the efficacy of drug treatments.
Highlights
Magnetic Resonance Imaging (MRI) offers the possibility to non-invasively assess the structure of the kidney as well as renal function in a single scan session
Data is presented from studies that use the multiparametric renal MRI protocol, comprising quantification of renal blood flow and perfusion, renal oxygenation, and markers of renal microstructural change due to fibrosis/inflammation
Variability, Repeatability, and Field Strength Dependence in Healthy Participants Here, we evaluate the variation in MRI measures within normal tissue of a healthy participant cohort, we assess renal artery and renal vein blood flow [as measured with phase contrast (PC)-MRI], kidney perfusion [as measured with arterial spin labeling (ASL)], T1 measures [and a comparison of readout schemes: spin echo–echo planar imaging (SE-EPI) and balanced fast field echo], tissue oxygenation, diffusion weighted imaging (DWI), and total kidney volume
Summary
Magnetic Resonance Imaging (MRI) offers the possibility to non-invasively assess the structure of the kidney as well as renal function in a single scan session. This article outlines the development of a quantitative functional multiparametric renal MRI protocol to probe hemodynamics (total and regional blood flow, perfusion), oxygenation [Blood Oxygen Level Dependent (BOLD) T2∗ imaging], and microstructure (diffusion weighted imaging, longitudinal relaxation time T1 mapping) and describes associated analysis methods. This multiparametric MRI protocol is applied in healthy participants, to assess both reproducibility and the field strength dependence of MRI parameters between 1.5 and 3 Tesla (T). This paper outlines a multiparametric renal MRI acquisition and analysis protocol to allow non-invasive assessment of hemodynamics (renal artery blood flow and perfusion), oxygenation (BOLD T2∗), and microstructure (diffusion, T1 mapping)
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