Atypical low-signal-intensity renal parenchyma: causes and patterns

Abstract

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.