Background
Gadolinium‐based contrast agents (GBCAs) are widely used in MRI, despite safety concerns regarding deposition in brain and other organs. In animal studies gadolinium was detected for weeks ...after administration in the kidneys, but this has not yet been demonstrated in humans.
Purpose
To find evidence for the prolonged presence of gadobutrol in the kidneys in healthy volunteers.
Study Type
Combined retrospective and prospective analysis of a repeatability study.
Population
Twenty‐three healthy volunteers with normal renal function (12 women, age range 40–76 years), of whom 21 were used for analysis.
Field Strength/Sequence
Inversion recovery‐based T1 map at 3T.
Assessment
T1 maps were obtained twice with a median interval of 7 (range: 4–16) days. The T1 difference (ΔT1) between both scans was compared between the gadolinium group (n = 16, 0.05 mmol/kg gadobutrol administered after T1 mapping during both scan sessions) and the control group (n = 5, no gadobutrol). T1 maps were analyzed separately for cortex and medulla.
Statistical Tests
Mann–Whitney U‐tests to detect differences in ΔT1 between groups and linear regression to relate time between scans and estimated glomerular filtration rate (eGFR) to ΔT1.
Results
ΔT1 differed significantly between the gadolinium and control group: median ΔT1 cortex –98 vs. 7 msec (P < 0.001) and medulla –68 msec vs. 19 msec (P = 0.001), respectively. The bias corresponds to renal gadobutrol concentrations of 8 nmol/g tissue (cortex) and 4 nmol/g tissue (medulla), ie, ~2.4 μmol for both kidneys (0.05% of original dose). ΔT1 correlated in the gadolinium group with duration between acquisitions for both cortex (regression coefficient (β) 16.5 msec/day, R2 0.50, P < 0.001) and medulla (β 11.5 msec/day, R2 0.32, P < 0.001). Medullary ΔT1 correlated with eGFR (β 1.13 msec/(ml/min) R2 0.25, P = 0.008).
Data Conclusion
We found evidence of delayed renal gadobutrol excretion after a single contrast agent administration in subjects with normal renal function. Even within this healthy population, elimination delay increased with decreasing kidney function.
Level of Evidence: 3
Technical Efficacy: Stage 3
J. Magn. Reson. Imaging 2020;52:622–631.
Increasing the concentration of oxygen dissolved in water is known to increase the recovery rate (R1 = 1/T1) of longitudinal magnetization (T1 relaxation). Direct T1 changes in response to precise ...hyperoxic gas challenges have not yet been quantified and the actual effect of increasing arterial oxygen concentration on the T1 of brain parenchyma remains unclear. The aim of this work was to use quantitative T1 mapping to measure tissue T1 changes in response to precisely targeted hyperoxic respiratory challenges ranging from baseline end-tidal oxygen (PetO2) to approximately 500 mmHg. We did not observe measureable T1 changes in either gray matter or white matter parenchymal tissue. The T1 of peripheral cerebrospinal fluid located within the sulci, however, was reduced as a function of PetO2. No significant T1 changes were observed in the ventricular cerebrospinal fluid under hyperoxia. Our results indicate that care should be taken to distinguish actual T1 changes from those which may be related to partial volume effects with cerebrospinal fluid, or regions with increased fluid content such as edema when examining hyperoxia-induced changes in T1 using methods based on T1-weighted imaging.
Purpose To provide insight into the effect of water T sub(1) relaxation (T sub(1wat)) on amide proton transfer (APT) contrast in tumors. Three different metrics of APT contrast-magnetization transfer ...ratio (MTR sub(Rex)), relaxation-compensated MTR sub(Rex) (AREX), and traditional asymmetry (MTR sub(asym))-were compared in normal and tumor tissues in a variety of intracranial tumors at 7 Tesla (T). Methods Six consented intracranial tumor patients were scanned using a low-power, three-dimensional (3D) APT imaging sequence. MTR sub(Rex) and MTR sub(asym) were calculated in the region of 3 to 4 ppm. AREX was calculated by T sub(1wat) correction of MTR sub(Rex). Tumor tissue masks, which classify different tumor tissues, were drawn by an experienced neuroradiologist. ROI-averaged tumor tissue analysis was done for MTR sub(Rex), AREX, and MTR sub(asym). Results MTR sub(Rex) and MTR sub(asym) were slightly elevated in tumor-associated structures. Both metrics were positively correlated to T sub(1wat). The correlation coefficient (R) was determined to be 0.88 (P < 0.05) and 0.92 (P << 0.05) for MTR sub(Rex) and MTR sub(asym), respectively. After T sub(1wat) correction (R = -0.21, P = 0.69), no difference between normal and tumor tissues was found for AREX. Conclusions The strong correlation of MTR sub(Rex) and MTR sub(asym) with T sub(1wat) and the absence thereof in AREX suggests that much of APT contrast in tumors for the low-power, 3D-acquisition scheme at 7 T originates from the inherent tissue water T sub(1)-relaxation properties. Magn Reson Med 77:1525-1532, 2017.
Imaging of the kidney using blood oxygen level dependent (BOLD) magnetic resonance imaging (MRI) presents a major opportunity to examine differences in tissue oxygenation within the cortex and ...medulla applicable to human disease. The aim of this study was to evaluate BOLD signals before and after treatment with RAS inhibitors in hypertensive chronic kidney disease (CKD) patients. Ten patients with stable CKD and 5 healthy volunteers were included. Five CKD patients were subjected to BOLD MRI scan before and after chronic treatment with 300 mg/day aliskiren for at least 6 weeks. Five other CKD patients received BOLD MRI before and 1 hour after acute treatment with 50 mg captopril. A group of healthy volunteers (n=5) was scanned before and 1 hour after acute treatment with 50 mg captopril. The 10 patients had a mean age of 61±17 years; eGFR of 30±11 mL/min per 1.73 m2. Office systolic and diastolic blood pressures when on a RAS inhibito, were 130±10 and 86±5 mmHg in CKD patients. Control subjects had normal kidney function and were not on any medication. In untreated condition, systolic and diastolic arterial blood pressure elevated, 145±6 and 95±4 mmHg, respectively. After chronic treatment with aliskiren, arterial blood pressure decreased in all patients in this group, 127±3 mmHg and 77±3 mmHg. After acute treatment with captopril arterial blood pressure reduced to 125±4 and 71±8 mmHg. Tissue intensity signal (T2*) was increased in medulla after chronic treatment from 29±6 to 34±6 and after acute treatment with captopril from 34±9 to 38±11 in CKD patients. In addition, T2* ratio between cortex and medulla decreased in CKD patients after chronic treatment and acute treatment. This ratio remained stable in healthy volunteers before and after treatment with captopril 1.62±0.1 and 1.65±0.1, respectively. This study shows for the first time that RAS inhibitors change BOLD signal in CKD patients. Importantly, in healthy volunteers, a RAS inhibitor had no such effect. Further investigation is required.
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