Multisection computed tomography (CT) was introduced in 1992 with the advent of dual-section-capable scanners and was improved in 1998 following the development of quad-section technology. With a recent increase in gantry speed from one to two revolutions per second, multisection CT scanners are now up to eight times faster than conventional single-section helical CT scanners. The benefits of quad-section CT relative to single-section helical CT are considerable. They include improved temporal resolution, improved spatial resolution in the z axis, increased concentration of intravascular contrast material, decreased image noise, efficient x-ray tube use, and longer anatomic coverage. These factors substantially increase the diagnostic accuracy of the examination. The multisection CT technique has enabled faster and superior evaluation of patients across a wide spectrum of clinical indications. These include isotropic viewing, musculoskeletal applications, use of multiplanar reformation in special situations, CT myelography, long coverage and multiphase studies, CT angiography, cardiac scoring, evaluation of brain perfusion, imaging of large patients, evaluation of acute chest pain or dyspnea, virtual endoscopy, and thin-section scanning with retrospective image fusing. Multisection CT is superior to single-section helical CT for nearly all clinical applications.

In ESRD patients, the factors correlating with coronary calcification were duration of dialysis and advancing age, whereas only age correlated with aorta calcification. Spiral CT offers an alternative technique for the assessment of these changes.

In this preliminary study, renal transplantation appears to slow down or arrest CAC, whereas CAC progresses in haemodialysis patients. In haemodialysis patients, CAC was greater in patients who died or were hospitalized compared with those who remained alive or were not hospitalized.

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Acquired and intrinsic resistance to receptor tyrosine kinase inhibitors (RTKi) represent a major hurdle in improving the management of clear cell renal cell carcinoma (ccRCC). Recent reports suggest that drug resistance is driven by tumor adaptation via epigenetic mechanisms that activate alternative survival pathways. The histone methyl transferase EZH2 is frequently altered in many cancers including ccRCC. To evaluate its role in ccRCC resistance to RTKi, we established and characterized a spontaneously metastatic, patient-derived xenograft (PDX) model that is intrinsically resistant to the RTKI sunitinib but not to the VEGF therapeutic antibody bevacizumab. Sunitinib maintained its anti-angiogenic and anti-metastatic activity but lost its direct anti-tumor effects due to kinome reprogramming, which resulted in suppression of pro-apoptotic and cell cycle regulatory target genes. Modulating EZH2 expression or activity suppressed phosphorylation of certain RTK, restoring the anti-tumor effects of sunitnib in models of acquired or intrinsically resistant ccRCC. Overall, our results highlight EZH2 as a rational target for therapeutic intervention in sunitinib-resistant ccRCC as well as a predictive marker for RTKi response in this disease.