Imaging description

Historically, prominent masslike foci of renal parenchyma simulating tumors were a well-recognized pitfall at intravenous pyelography, but such pseudotumors can also be seen at ultrasound and sometimes CT. Masslike foci of renal parenchyma may be congenital or acquired, and causes include a hypertrophied column of Bertin, lobar dysmorphism, persistent fetal lobation, dromedary or splenic hump, and scarring with focal sparing or compensatory hypertrophy (Figures 43.1–43.4) [1–9]. In 1744, the French anatomist Exupere Joseph Bertin noted that the renal cortex not only envelops the kidney, but also extends in radial bands between the medullary pyramids. These radial bands are now known as the septa or columns of Bertin [1]. When unusually thickened, they are said to be hypertrophied and may mimic a mass. As insightfully noted by Yeh et al., the tissue is not actually hypertrophied, but rather reflects incomplete fusion of the fetal lobes or sub-kidneys that normally join together to form the kidney during gestation and arguably would be more correctly termed “junctional parenchyma” [3]. Renal lobar dysmorphism is a related congenital anomaly in which a diminutive lobe develops between two normal lobes. It resembles a hypertrophied column of Bertin, except that it also contains medullary tissue [4]. Fetal lobation is another form of incomplete lobar fusion in which persistent grooves in the renal outline demarcate the junction between fetal lobes [5]. The tissue between these grooves may sometimes appear masslike.