Quantitative magnetic resonance imaging of chronic kidney disease: an experimental in vivo study using rat chronic kidney disease models

Background Recent advances in magnetic resonance imaging (MRI) may allow it to be an alternative emerging tool for the non-invasive evaluation of renal parenchymal disease. Purpose To validate the usefulness of quantitative multiparametric MRI protocols and suggest the suitable quantitative MR sequence protocol to evaluate parenchymal fibrosis using an animal model of chronic kidney disease (CKD) by long-term adenine intake. Material and Methods In this prospective animal study, 16 male Wistar rats were analyzed and categorized into three groups. Rats in the CKD groups underwent 0.25% adenine administration for three or six weeks. Quantitative MRI protocols, including diffusion-weighted imaging (DWI), T1ρ (T1 rho), and T2* mapping were performed using a 9.4-T animal MR scanner. A semi-quantitative histopathologic analysis for renal fibrosis was conducted. Quantitative MR values measured from anatomic regions of kidneys underwent intergroup comparative analyses. Results The apparent diffusion coefficient (ADC) and T1 (T1 rho) values were significantly increased in all CKD groups. Values measured from the cortex and outer medulla showed significant intergroup differences. Total ADC values tended to increase according to periods, and T1ρ values increased in three weeks and decreased in six weeks. Conclusion Quantitative MRI protocols could be a non-invasive assessment modality in the diagnosis and evaluation of CKD. Particularly, T1ρ may be a suitable MR sequence to quantitatively assess renal parenchymal fibrosis.

Cutoff points of T1 rho / T2 mapping relaxation times distinguishing early-stage and advanced osteoarthritis

IntroductionThe histopathology grading system is the gold post-operative method to evaluate cartilage degeneration in knee osteoarthritis (OA). Magnetic resonance imaging (MRI) T1 rho/T2 mapping imaging can be used as a preoperative detection. An association between histopathology and T1 rho/T2 mapping relaxation times value was suggested in previous research. However, the cutoff point was not determined among different histopathology grades. Our study was to discuss the cutoff point of T1 rho/T2 mapping.Material and methodsT1 rho/T2 mapping images were acquired from 80 samples before total knee replacements. Then the histopathology grading system was applied.ResultsThe mean T1 rho/T2 mapping relaxation times of 80 samples were 39.17 ms and 37.98 ms respectively. Significant differences were found in T1 rho/T2 mapping values between early-stage and advanced OA (P < 0.001). The cutoff point for T1 rho was at 33 ms with a sensitivity of 94.12 (95%CI: 80.3 to 99.3) and a specificity of 91.30 (95%CI: 79.2 to 97.6). The cutoff point for T2 mapping was suggested at 35.04 ms with a sensitivity of 88.24 (95%CI: 72.5 to 96.7) and specificity of 97.83 (95%CI: 88.5 to 99.9). After bootstrap simulation, 95% CI of T1 rho/T2 mapping cutoff point was estimated as 29.36 to 36.32 ms and 34.8 to 35.04 ms respectively. The area under PR curve of T1 rho/T2 mapping was 0.972 (95%CI: 0.925 to 0.992) and 0.949 (95%CI: 0.877 to 0.989) respectively.ConclusionsThe cutoff point of T1 rho relaxation times, which was suggested as 33 ms could be used to distinguish early-stage and advanced OA.

Subcortical T1-Rho MRI Abnormalities in Juvenile-Onset Huntington’s Disease

Huntington’s disease (HD) is a fatal neurodegenerative disease caused by the expansion of cytosine-adenine-guanine (CAG) repeats in the huntingtin gene. An increased CAG repeat length is associated with an earlier disease onset. About 5% of HD cases occur under the age of 21 years, which are classified as juvenile-onset Huntington’s disease (JOHD). Our study aims to measure subcortical metabolic abnormalities in JOHD participants. T1-Rho (T1ρ) MRI was used to compare brain regions of 13 JOHD participants and 39 controls. Region-of-interest analyses were used to assess differences in quantitative T1ρ relaxation times. We found that the mean relaxation times in the caudate (p < 0.001), putamen (p < 0.001), globus pallidus (p < 0.001), and thalamus (p < 0.001) were increased in JOHD participants compared to controls. Furthermore, increased T1ρ relaxation times in these areas were significantly associated with lower volumes amongst participants in the JOHD group. These findings suggest metabolic abnormalities in brain regions previously shown to degenerate in JOHD. We also analyzed the relationships between mean regional T1ρ relaxation times and Universal Huntington’s Disease Rating Scale (UHDRS) scores. UHDRS was used to evaluate participants’ motor function, cognitive function, behavior, and functional capacity. Mean T1ρ relaxation times in the caudate (p = 0.003), putamen (p = 0.005), globus pallidus (p = 0.009), and thalamus (p = 0.015) were directly proportional to the UHDRS score. This suggests that the T1ρ relaxation time may also predict HD-related motor deficits. Our findings suggest that subcortical metabolic abnormalities drive the unique hypokinetic symptoms in JOHD.

Abstract TP60: T1 Rho Magnetic Resonance Imaging Can Detect and Quantify Acute Ischemic Stroke in Humans

Introduction: Establishing a timeline of acute ischemic stroke (AIS) onset is critically important for selecting time-sensitive treatments. However, there is currently no accepted imaging method for reliably dating stroke onset. T1 Rho MR is an investigative imaging modality for quantifying the spin lattice relaxation time constant in a rotating frame. T1 Rho is sensitive to chemical exchange, and in acute stroke, has been shown in animal models to increase linearly in the first 6 hours after onset of cerebral infarction, making it possible to accurately date onset. Hypothesis: We hypothesize that a rapid non-contrast T1 Rho MR sequence can be used to detect and quantify AIS in humans. Methods: AIS patients (n=11) underwent 3.0T brain MR scans in the late acute to subacute period after onset (mean 56 hours). The infarct volume was identified on DWI and infarct regions of interest (ROIs) were mapped onto the contralateral side to serve as within-subject controls. Infarct and control ROIs were co-registered with T1 Rho maps and compared using a Student t-test. Results: T1 Rho infarct volume correlated well to DWI volume and mean T1 Rho intensity values in the infarct, were significantly higher compared to controls (p<0.004, mean difference 37ms, std 19.3). When inter-individual T1rho values were plotted against time from stroke onset, we found that they remained stable. Conclusion: T1 Rho MR is feasible, and can detect and quantify AIS in humans. Further, T1 Rho values in the infarct bed were stable in the late acute to early subacute time period, consistent with animal studies that show T1rho values to undergo predictable change only in the first 6 hours after infarct onset. Further studies are needed to determine if T1rho in humans has a predicable rate of change in the early acute phase, that can one day be used as a quantifiable surrogate of stroke onset and thus inform stroke therapy when time of onset is unknown.