Background Sodium-23 magnetic resonance imaging (23Na MRI) allows direct measurement of tissue sodium concentrations. Current knowledge of skin, muscle and bone sodium concentrations in chronic kidney disease (CKD) and renal replacement therapy patients is limited. In this study we measured the tissue sodium concentrations in CKD, hemodialysis (HD) and peritoneal dialysis (PD) patients with 23Na MRI of the lower leg and explored their correlations with established clinical biomarkers. Methods Ten healthy controls, 12 CKD Stages 3–5, 13 HD and 10 PD patients underwent proton and 23Na MRI of the leg. The skin, soleus and tibia were segmented manually and tissue sodium concentrations were measured. Plasma and serum samples were collected from each subject and analyzed for routine clinical biomarkers. Tissue sodium concentrations were compared between groups and correlations with blood-based biomarkers were explored. Results Tissue sodium concentrations in the skin, soleus and tibia were higher in HD and PD patients compared with controls. Serum albumin showed a strong, negative correlation with soleus sodium concentrations in HD patients (r = −0.81, P < 0.01). Estimated glomerular filtration rate showed a negative correlation with tissue sodium concentrations (soleus: r = −0.58, P < 0.01; tibia: r = −0.53, P = 0.01) in merged control–CKD patients. Hemoglobin was negatively correlated with tissue sodium concentrations in CKD (soleus: r = −0.65, P = 0.02; tibia: r = −0.73, P < 0.01) and HD (skin: r = −0.60, P = 0.04; tibia: r = −0.76, P < 0.01). Conclusion Tissue sodium concentrations, measured by 23Na MRI, increase in HD and PD patients and may be associated with adverse metabolic effects in CKD and dialysis.
In this brief report, computed tomography perfusion (CTP) thresholds predicting follow-up infarction in patients presenting 20 to 23 seconds and cerebral blood flow <5 to 7 ml/min-1/(100 g)-1 or relative cerebral blood flow <0.14 to 0.20 optimally predicted the final infarct. These thresholds are stricter than published thresholds.
Background and Purpose-Intracerebral hemorrhage is a feared complication of intravenous alteplase therapy in patients with acute ischemic stroke. We explore the use of multimodal computed tomography in predicting this complication. Methods-All patients were administered intravenous alteplase with/without intra-arterial therapy. An age-and sex-matched case-control design with classic and conditional logistic regression techniques was chosen for analyses. Outcome was parenchymal hemorrhage on 24-to 48-hour imaging. Exposure variables were imaging (noncontrast computed tomography hypoattenuation degree, relative volume of very low cerebral blood volume, relative volume of cerebral blood flow ≤7 mL/min•per 100 g, relative volume of T max ≥16 s with all volumes standardized to z axis coverage, mean permeability surface area product values within T max ≥8 s volume, and mean permeability surface area product values within ipsilesional hemisphere) and clinical variables (NIHSS [National Institutes of Health Stroke Scale], onset to imaging time, baseline systolic blood pressure, blood glucose, serum creatinine, treatment type, and reperfusion status). Results-One-hundred eighteen subjects (22 patients with parenchymal hemorrhage versus 96 without, median baseline NIHSS score of 15) were included in the final analysis. In multivariable regression, noncontrast computed tomography hypoattenuation grade (P<0.006) and computerized tomography perfusion white matter relative volume of very low cerebral blood volume (P=0.04) were the only significant variables associated with parenchymal hemorrhage on follow-up imaging (area under the curve, 0.73; 95% confidence interval, 0.63-0.83). Interrater reliability for noncontrast computed tomography hypoattenuation grade was moderate (κ=0.6). Conclusions-Baseline hypoattenuation on noncontrast computed tomography and very low cerebral blood volume on computerized tomography perfusion are associated with development of parenchymal hemorrhage in patients with acute ischemic stroke receiving intravenous alteplase.
Background and Aims High flux dialysis membranes sufficiently remove smaller sized uremic toxins however, the accumulation and retention of larger middle molecular weight toxins, which are associated with chronic inflammation, cardiovascular disease and suboptimal outcomes are poorly cleared. The recent advent of medium-cut-off dialysis membranes, labelled “expanded dialysis” (HDx) are permeable to molecules of larger size responsible for poor clinical outcomes. However, it remains unclear if HDx can directly impact the symptoms associated with hemodialysis (HD). Symptom burden plays a significant role in quality of life (QOL) and mortality rates in the HD population. The London Evaluation of Illness (LEVIL), an application-based platform has been developed to measure patient reported outcomes (PROM). In comparison to cross-sectional PROM’s, LEVIL more accurately represents the fluctuations in daily symptoms and the impact of intervention. LEVIL evaluates general well-being, energy, sleep, appetite, pain and breathing, all of which are outcomes of interest on symptom burden in chronic kidney disease. Our aim was to determine if HDx therapy had any effect on symtoms/QOL domains using LEVIL. Method 28 patients from two dialysis centers in London Ontario were consented to participate. Patients were required to be over 18 years of age and on conventional thrice weekly maintenance HD for at least three months. 23 participants completed study and analyzed (five lost for various reasons). Baseline (BL) symptom characteristics were obtained while using high flux membrane for two weeks. Symptoms continued to be measured throughout the 12 weeks of HDx therapy two-three times weekly using LEVIL. Laboratory biomarkers including beta-2 microglobulin and free-light chains were collected at baseline and after 12 weeks of HDx therapy. Results Patients were stratified into tertiles (high/middle/low) using mean values of BL symptoms scores in each domain (wellbeing, energy, sleep, appetite, pain, breathing). Those in the high BL group were labeled as “control”. Low and middle BL measures were further stratified into responders vs. non-responders (responders were considered to have a 50% increase in any symptom domain by ≥50%). Of those domains which responded to HDx, 76% also had low BL scores with 27% having middle BL scores. General wellbeing, energy and sleep were domains with the greatest response reaching statistical significance after eight weeks of therapy. HDx had limited effect on appetite, pain and breathing. Although stratification was per domain, overall, 74% of the population studied did respond in at least one domain, with some responding in as many as five. Conclusion HDx using Theranova (Baxter) shows the most benefit in domains with low BL measures. Additionally, not everyone who had low BL scores responded after 12 weeks of therapy, leaving us to question whether HDx may have a latent effect in some individuals/populations. Those who had no response to therapy in certain domains also had greater baseline quality of life respectively. This information may assist in decision making/rationale for the utilization and implementation of such therapy. Although more work is required to further stratify symptoms in relation to demographic/biochemical finding and clinical outcomes. It is evident that HDx improves patient reported symptoms and QOL.
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