Massive renal infarction with perirenal hematoma formation occurring in sickle-cell trait has not been previously reported. Various renal complications in patients with sickle-cell trait have been described by Harrow (5), Kay (6), and Vix (13), but no cases of extensive renal infarction were included. The present report describes infarction of the kidney and demonstrates the radiographic features of perirenal hematoma in the sickle-cell trait. The association of sickle-cell hemoglobinopathy and hematuria was first reported by Goodwin in 1950. Since then hematuria and renal papillary necrosis have been described in hemoglobin SA, SC, and SD disease (5, 6, 13). Gunnells and Grim (4), reporting hematuria in AD hemoglobinopathy, emphasized that hemoglobinopathies must be considered in cases of “essential” or “unexplained” hematuria. Case Report A 33-year-old Negro laborer was hospitalized with right upper quadrant abdominal pain of twelve hours duration. During the preceding two years the patient had experienced five similar episodes of pain which usually lasted twenty-four hours and had been treated with aspirin by the patient. There was no family history of sickle-cell anemia. On physical examination right costovertebral and right upper quadrant tenderness were present, and there was a questionable right upper quadrant mass. The bowel sounds were active. Hematuria was present. Radiographic studies on admission suggested a mass in the right upper quadrant and a bone infarct in the left femoral head (Fig. 1). Intravenous urography the same day demonstrated a nonfunctioning right kidney. Retrograde pyelography the next morning showed extensive hydronephrosis on the right (Fig. 2) and a renal arteriogram the same afternoon, approximately forty to forty-four hours after the initial symptoms, showed two patent right renal arteries. The small peripheral vessels were irregular, however, with markedly attenuated distal segments (Fig. 3). A nephrogram density was visualized within the large nonopacified mass in the right upper quadrant. The mass was considered to represent a perirenal hematoma secondary to either trauma or cortical infarct with subsequent capsular rupture. The patient denied any flank trauma, but in view of the bone infarct it was suggested that sickling might be responsible for a renal cortical infarct. A sickle test was positive, and hemoglobin electrophoresis revealed hemoglobin A—61.8 per cent, hemoglobin S—36 per cent, hemoglobin A 2—1 per cent, hemoglobin F—1.2 per cent. At surgery stenosis of the ureteropelvic junction was found, explaining the marked hydronephrosis. A large perirenal hematoma surrounding the kidney was evacuated and a right nephrectomy performed. Pathological examination revealed chronic and active pyelonephritis as well as sickled cells in the glomerular capillaries.