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Over the past decade, computed tomographic (CT) urography has emerged as the primary imaging modality for evaluating the urinary tract in various clinical settings, including the initial workup of hematuria. With the widespread implementation of CT urography, it is critical for radiologists to understand normal ureteral anatomy and the varied appearance of pathologic ureteral conditions at CT urography. Pathologic findings at CT urography include congenital abnormalities, filling defects, dilatation, narrowing, and deviations in course. These abnormalities are reviewed, along with the indications for CT urography, current imaging protocols with specific techniques for optimal evaluation of the ureter, and dose reduction strategies., ((©)RSNA, 2015.)

Fibroblasts are key mediators of fibrosis in the kidney and other organs, but their origin during fibrosis is still not completely clear. Activated fibroblasts likely arise from resident quiescent fibroblasts via epithelial-to-mesenchymal transition and from the bone marrow. Here, we demonstrate that endothelial cells also contribute to the emergence of fibroblasts during kidney fibrosis via the process of endothelial-to-mesenchymal transition (EndMT). We examined the contribution of EndMT to renal fibrosis in three mouse models of chronic kidney disease: (1) Unilateral ureteral obstructive nephropathy, (2) streptozotocin-induced diabetic nephropathy, and (3) a model of Alport renal disease. Approximately 30 to 50% of fibroblasts coexpressed the endothelial marker CD31 and markers of fibroblasts and myofibroblasts such as fibroblast specific protein-1 and alpha-smooth muscle actin. Endothelial lineage tracing using Tie2-Cre;R26R-stop-EYFP transgenic mice further confirmed the presence of EndMT-derived fibroblasts. Collectively, our results demonstrate that EndMT contributes to the accumulation of activated fibroblasts and myofibroblasts in kidney fibrosis and suggest that targeting EndMT might have therapeutic potential.