BackgroundDapagliflozin inhibits the sodium‐glucose–linked transporter 2 in the renal proximal tubule, thereby promoting glycosuria to reduce hyperglycemia in type 2 diabetes mellitus. Because these patients may require loop diuretics, and sodium‐glucose–linked transporter 2 inhibition causes an osmotic diuresis, we evaluated the diuretic interaction between dapagliflozin and bumetanide.Methods and ResultsHealthy subjects (n=42) receiving a fixed diet with ≈110 mmol·d−1 of Na+ were randomized to bumetanide (1 mg·d−1), dapagliflozin (10 mg·d−1), or both for 7 days, followed by 7 days of both. There were no meaningful pharmacokinetic interactions. Na+ excretion increased modestly with the first dose of dapagliflozin (22±6 mmol·d−1; P<0.005) but by more (P<0.005) with the first dose of bumetanide (74±7 mmol·d−1; P<0.005), which was not significantly different from both diuretics together (80±5 mmol·d−1; P<0.005). However, Na+ excretion with dapagliflozin was 190% greater (P<0.005) when added after 1 week of bumetanide (64±6 mmol·d−1), and Na+ excretion with bumetanide was 36% greater (P<0.005) when added after 1 week of dapagliflozin (101±8 mmol·d−1). Serum urate was increased 4% by bumetanide but reduced 40% by dapagliflozin or 20% by combined therapy (P<0.05).ConclusionsFirst‐dose Na+ excretion with bumetanide and dapagliflozin is not additive, but the weekly administration of one diuretic enhances the initial Na+ excretion with the other, thereby demonstrating mutual adaptive natriuretic synergy. Combined therapy reverses bumetanide‐induced hyperuricemia. This requires further study in diabetic patients with hyperglycemia who have enhanced glycosuria and natriuresis with dapagliflozin.Clinical Trial RegistrationURL: http://www.clinicaltrials.gov. Unique identifier: NCT00930865.

Combined IVIM and ASL MRI can better evaluate the diffusion and perfusion properties for allografts early after kidney transplantation.

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ObjectiveTo investigate the liver T1rho values for detecting fibrosis, and the potential impact of fatty liver on T1rho measurements.Materials and MethodsThis study included 18 healthy subjects, 18 patients with fatty liver, and 18 patients with liver fibrosis, who underwent T1rho MRI and mDIXON collections. Liver T1rho, proton density fat fraction (PDFF) and T2* values were measured and compared among the three groups. Receiver operating characteristic (ROC) curve analysis was performed to evaluate the T1rho values for detecting liver fibrosis. Liver T1rho values were correlated with PDFF, T2* values and clinical data.ResultsLiver T1rho and PDFF values were significantly different (p < 0.001), whereas the T2* (p = 0.766) values were similar, among the three groups. Mean liver T1rho values in the fibrotic group (52.6 ± 6.8 ms) were significantly higher than those of healthy subjects (44.9 ± 2.8 ms, p < 0.001) and fatty liver group (45.0 ± 3.5 ms, p < 0.001). Mean liver T1rho values were similar between healthy subjects and fatty liver group (p = 0.999). PDFF values in the fatty liver group (16.07 ± 10.59%) were significantly higher than those of healthy subjects (1.43 ± 1.36%, p < 0.001) and fibrosis group (1.07 ± 1.06%, p < 0.001). PDFF values were similar in healthy subjects and fibrosis group (p = 0.984). Mean T1rho values performed well to detect fibrosis at a threshold of 49.5 ms (area under the ROC curve, 0.855), had a moderate correlation with liver stiffness (r = 0.671, p = 0.012), and no correlation with PDFF, T2* values, subject age, or body mass index (p > 0.05).ConclusionT1rho MRI is useful for noninvasive detection of liver fibrosis, and may not be affected with the presence of fatty liver.

Purpose To determine the relationship between diffusion-weighted imaging (DWI) and diffusion kurtosis imaging (DKI) in patients with acute stroke at admission and the tissue outcome 1 month after onset of stroke. Materials and Methods Patients with stroke underwent DWI (b values = 0, 1000 sec/mm along three directions) and DKI (b values = 0, 1000, 2000 sec/mm along 20 directions) within 24 hours after symptom onset and 1 month after symptom onset. For large lesions (diameter ≥ 1 cm), acute lesion volumes at DWI and DKI were compared with those at follow-up T2-weighted imaging by using Spearman correlation analysis. For small lesions (diameter < 1 cm), the number of acute lesions at DWI and DKI and follow-up T2-weighted imaging was counted and compared by using the McNemar test. Results Thirty-seven patients (mean age, 58 years; range, 35-82 years) were included. There were 32 large lesions and 138 small lesions. For large lesions, the volumes of acute lesions on kurtosis maps showed no difference from those on 1-month follow-up T2-weighted images (P = .532), with a higher correlation coefficient than those on the apparent diffusion coefficient and mean diffusivity maps (R = 0.730 vs 0.479 and 0.429). For small lesions, the number of acute lesions on DKI, but not on DWI, images was consistent with that on the follow-up T2-weighted images (P = .125). Conclusion DKI complements DWI for improved prediction of outcome of acute ischemic stroke. RSNA, 2018.

Magnetic quantum dots (MQDs) are an important class of agents for fluorescence (FL)/magnetic resonance (MR) dual-modal imaging due to their excellent optical and magnetic properties. However, functional MQDs prepared by a simple room-temperature route as FL/MR dual-modal imaging probes are lacking.Herein, we report the fabrication of Gd-doped CdTe quantum dots (Gd:CdTe QDs) as an agent for FL/MR dual-modality imaging. The as-designed QDs with an ultrasmall particle size are synthesized by a facile one-pot aqueous synthesis approach at room temperature. They emit strong fluorescence at 640 nm with a quantum yield of 37% in water, and they have a high longitudinal relaxation rate (r 1 ) value of 3.27 mM À1 s À1 . With the further conjugation of folic acid, the Gd:CdTe QDs can successfully label live HepG2 cells for targeted cellular imaging and present no evidence of cellular toxicity up to the concentration of 0.5 mg mL À1 . They have been employed as a suitable contrast agent successfully for tumor-targeted FL/MR dual-modal imaging in a mouse model.

The aim of this study was to explore the risk factors associated with longitudinal changes in hemodialysis patients including the correlation between number and distribution of cerebral microbleeds (CMBs).Sixty-one hemodialysis patients were enrolled in this prospective study. Twenty-eight patients had follow-up examinations with a mean interval of 24.79 ± 5.17 months. The number of CMBs was manually counted on susceptibility-weighted imaging. Subjects were divided into 2 groups with and without CMBs. In the CMB group, 8 of 33 patients did not have a mini-mental state examination (MMSE) because of blurred vision. Multiple logistic regression was used to investigate the risk factors for CMBs. Partial correlation was used to explore the correlation between the increased number of CMBs and the change of MMSE scores.CMBs were seen in 33 (54%) hemodialysis patients. Both age and pre/postdialysis systolic blood pressure (SBP) positively correlated with CMBs. Serum iron (SI), and high-density lipoprotein cholesterol (HDL-c) negatively correlated with CMBs (all P < 0.05). Among 25 patients with CMBs and MMSE, 9 patients had scores <27, which was considered as subnormal and most CMBs in these patients were located in the brainstem and basal ganglia. Considering age and follow-up time as the co-confounding factors, the number of new CMBs over the 2 imaging time points negatively correlated with the change of MMSE scores (r = −0.673, P = 0.023).The presence of new CMBs was a risk factor for cognitive dysfunction and the location of CMBs may be correlated with cognitive impairment. Both SI and HDL-c were protective factors for the CMBs. The risk factors for CMBs included age, pre- and postdialysis SBP.

• DTI and tractography can evaluate renal allograft function at an early stage • Medullary FA, cortical and medullary ADC can effectively evaluate allograft function • Medullary FA, cortical and medullary ADC are correlated with eGFR in renal allografts • Medullary ADC increased and cortical FA decreased in stable allografts compared to control subjects • Medullary FA, cortical and medullary ADC decreased and allograft function declined.