Atypical Low-Signal-Intensity Renal Parenchyma: Causes and Patterns
Jun Yong Jeong, MD ; Seung Hyup Kim, MD ; Hak Jong Lee, MD ; Jung Suk Sim, MD

1 From the Department of Radiology and Institute of Radiation Medicine, Seoul National University College of Medicine, 28 Yongon-dong, Chongno-gu, Seoul 110-744, Korea; and the Clinical Research Institute, Seoul National University Hospital. Presented as an education exhibit at the 2000 RSNA scientific assembly. Received June 8, 2001; revision requested July 17; final revision received February 12, 2002; accepted February 28. Supported in part by the 2000 BK21 Project for Medicine, Dentistry, and Pharmacy.

Certain renal diseases manifest as low signal intensity of the renal parenchyma on magnetic resonance images. Sometimes, the appearance is sufficiently characteristic to allow a specific radiologic diagnosis to be made. The causes of this finding can be classified into three main categories on the basis of the pathophysiology: hemolysis, infection, and vascular disease. The first category includes paroxysmal nocturnal hemoglobinuria (PNH), hemosiderin deposition in the renal cortex from mechanical hemolysis, and sickle cell disease. The second category includes hemorrhagic fever with renal syndrome (HFRS). The third category includes acute renal vein thrombosis, renal cortical necrosis, renal arterial infarction, rejection of a transplanted kidney, and acute nonmyoglobinuric renal failure with severe loin pain and patchy renal vasoconstriction. These disease processes have different patterns of low signal intensity. PNH, hemosiderin deposition from mechanical hemolysis, and sickle cell disease involve the entire cortex including the columns of Bertin. HFRS involves the medulla, especially the outer medulla, whereas cortical necrosis involves the inner cortex including the columns of Bertin. In renal vein thrombosis, low-signal-intensity lesions involve the outer medulla, an appearance resembling that of HFRS. Wedge-shaped low-signal-intensity regions involving both the cortex and the medulla are seen in arterial infarction.