Introduction

Sickle cell anemia (SCA) is a disease caused by production of abnormal hemoglobin, which binds with other abnormal hemoglobin molecules within the red blood cell to cause rigid deformation of the cell. This deformation impairs the ability of the cell to pass through small vascular channels; sludging and congestion of vascular beds may result, followed by tissue ischemia and infarction. Infarction is common throughout the body in the patient with SCA, and it is responsible for the earliest clinical manifestation, the acute pain crisis, which is thought to result from marrow infarction. Over time, such insults result in medullary bone infarcts and epiphyseal osteonecrosis. In the brain, white matter and gray matter infarcts are seen, causing cognitive impairment and functional neurologic deficits. The lungs are also commonly affected, with infarcts, emboli (from marrow infarcts and fat necrosis), and a markedly increased propensity for pneumonia. The liver, spleen, and kidney may experience infarction as well. An unusual but life-threatening complication of SCA is sequestration syndrome, wherein a considerable amount of the intravascular volume is sequestered in an organ (usually the spleen), causing vascular collapse; its pathogenesis is unknown. Finally, because the red blood cells are abnormal, they are removed from the circulation, resulting in a hemolytic anemia. For the patient with SCA, however, the ischemic complications of the disease far outweigh the anemia in clinical importance.

The language of radiology is rich with descriptions of imaging findings, often metaphorical, which have found common usage in the day-to-day practice of genitourinary radiology. These "classic signs" give us confidence in our diagnosis. Some of the signs have become so familiar to us that they are referred to as an "Aunt Minnie." When the sign is invoked, or an Aunt Minnie is recognized, it often brings an impression of the image to mind, and it may have specific diagnostic and pathologic implications. The article uses classic signs accumulated from the literature to review a variety of pathologic conditions in the urinary tract. Copyright RSNA, 2004.

Renal papillary necrosis is not a pathologic entity but rather a descriptive term for a condition--necrosis of the renal papillae--that has various possible causes. The renal medulla and papillae are vulnerable to ischemic necrosis because of the peculiar arrangement of their blood supply and the hypertonic environment. The etiology of renal papillary necrosis includes diabetes, analgesic abuse or overuse, sickle cell disease, pyelonephritis, renal vein thrombosis, tuberculosis, and obstructive uropathy. Renal papillary necrosis has been diagnosed with the use of intravenous urography and ultrasonography, but contrast material-enhanced computed tomography (CT) may better depict a full range of typical features, including contrast material-filled clefts in the renal medulla, nonenhanced lesions surrounded by rings of excreted contrast material, and hyperattenuated medullary calcifications. In the presence of papillary sloughing, CT may depict hydronephrosis and filling defects in the renal pelvis or ureter, which also may contain calcifications. During healing, the epithelialized papillary tip appears blunted. Shrinkage of the kidney, a common sequela, also may be detected at CT. Multi-detector row CT depicts these and other features more clearly and directly than single-detector row CT, given the advantages of thinner sections and multiplanar reformation, and it may help identify the condition at an earlier stage, when effective treatment can reverse the ischemic process. Familiarity with the CT features of the condition therefore is useful for its successful diagnosis and management. RSNA, 2006