Multilayer stent appeared to be an acceptable treatment option for primary infected juxtarenal aortic aneurysms. Aneurysmal sac completely disappeared and visceral branches remained patent at 2-year follow-up. However, longer follow-up is necessary to evaluate the long-term patency of involved visceral arteries.
Background and aims
Chronic kidney disease (CKD) is strongly associated with a high burden of cardiovascular morbidity and mortality. Therefore, we aimed to characterize the putative role of microRNAs (miR)s in uremic vascular remodelling and endothelial dysfunction.
Methods
We investigated the expression pattern of miRs in two independent end-stage renal disease (ESRD) cohorts and in the animal model of uremic DBA/2 mice
via
quantitative RT-PCR. Moreover, DBA/2 mice were treated with intravenous injections of synthetic miR-142-3p mimic and were analysed for functional and morphological vascular changes by mass spectrometry and wire myography.
Results
The expression pattern of miRs was regulated in ESRD patients and was reversible after kidney transplantation. Out of tested miRs, only blood miR-142-3p was negatively associated with carotid-femoral pulse-wave velocity in CKD 5D patients. We validated these findings in a murine uremic model and found similar suppression of miR-142-3p as well as decreased acetylcholine-mediated vascular relaxation of the aorta. Therefore, we designed experiments to restore bioavailability of aortic miR-142-3p
in vivo
via intravenous injection of synthetic miR-142-3p mimic. This intervention restored acetylcholine-mediated vascular relaxation.
Conclusions
Taken together, we provide compelling evidence, both in humans and in mice, that miR-142-3p constitutes a potential pharmacological agent to prevent endothelial dysfunction and increased arterial stiffness in ESRD.
With prostate and colorectal malignancies being the most common cancers in men, elevated prostate specific antigen (PSA) in patients without rectal access due to prior surgery poses a diagnostic dilemma. We report the first use of CT-guided biopsy in combination with prebiopsy MRI in 2 patients with a clinical suspicion of prostate cancer and no rectal access. In both cases, a diagnostic multiparametric MRI of the prostate was performed to detect and to localize a potential suspicious lesion. The localization served as a cognitive map for guiding needle placement using a CT-guided transgluteal approach.
Vascular calcification is a frequent complication of chronic kidney disease and end stage renal disease. In both the general population and patients with end stage renal disease, vascular calcification is related to arterial stiffness and is a predictor of cardiovascular morbidity and mortality. Various diagnostic methods are currently used to assess vascular calcification. There is a preference for simple, reliable methods that can be used in daily practice. Therefore, several imaging and laboratory methods are investigated. Twenty-eight patients with mean age of 62 years on chronic hemodialysis were enrolled in the study. The mean duration of hemodialysis treatment was 70 months (range 3 to 350 months). Vascular calcification was assessed with coronary computed tomography and lateral lumbar, pelvic and hand radiographs. Vascular stiffness was evaluated using aortic pulse wave velocity and ankle-brachial index measurements, and finally serum levels of fibroblast growth factor-23 were followed. A statistically significant correlation was demonstrated between all the following parameters: coronary artery calcification score, aortic pulse wave velocity, abdominal aortic calcification score, simple vascular calcification scores in pelvis and hand. A statistically significant correlation of ankle-brachial index >1.3 to coronary artery calcification score was found. There was no correlation between the previous parameters and fibroblast growth factor-23. The results of our study indicate that simple imaging methods could provide confident vascular damage assessment and therefore potentially guide therapy adjustments. An association between fibroblast growth factor-23 and the other diagnostic modalities in our study was not found.
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