Several recent articles in the urologic literature (11, 13, and 14) have pointed out that infarction of the kidney is a definite clinical entity which is capable of accurate diagnosis. Despite this, instances of its correct clinical recognition are infrequent (8). Here the radiologist has a major role to play, since under some circumstances an almost certain diagnosis can be reached on roentgen grounds alone and, on other occasions, the radiographic findings may be strongly suggestive. The present report is based on 13 cases of renal infarction, with adequate radiographic work-up, seen at the Syracuse Medical Center Hospitals in the last eight years. In 7 of this number, the diagnosis was confirmed at surgery or autopsy, and in 1 by aortography. In 5, the history, roentgen findings, and subsequent course, with return of function to the involved kidney in 3 instances, were considered proof of infarction (Table I). Etiology Arterial occlusion leading to renal infarction may result from thrombosis, embolus, or trauma. Embolism is said to be the most common etiologic factor (11, 13). Hoxie and Coggin (8) report that 76 per cent of 205 patients were found to have cardiac lesions at autopsy. Regan and Crabtree (13) found cardiac or vascular lesions in 34 of 47 cases of renal arterial occlusion and state that embolism to the kidney occurs in about 25 per cent of cases of subacute bacterial endocarditis. According to Lynch (9), many patients have a past history of myocardial infarction. Instances of renal artery thrombosis are most often secondary to atherosclerosis, but surgical trauma to the renal pedicle (11) and polycythemia (10) are occasional causal factors. Occlusion secondary to trauma is rare. The finding of renal infarction without demonstrable occlusion of the renal artery has been reported. To explain this phenomenon, Lynch gives clinical and experimental evidence to suggest that infarction may at times be secondary to arterial spasm. Renal vein thrombosis most commonly occurs secondary to adjacent neoplasm, but, under such circumstances, acute symptoms rarely develop. Acute renal vein thrombosis is found most frequently in septic states, often in debilitated patients. Most of the previously recorded cases have been in children (4, 12, 13). Symptomatology The usual history of acute renal arterial occlusion is one of abrupt onset of abdominal or flank pain, gradually subsiding in seven to ten days, in a patient with cardiac or vascular disease. Nausea and vomiting occur in about half the cases. Fever and leukocytosis are common in the first twenty-four hours and are related to tissue death. Albuminuria is almost always present, and hematuria is seen in 50 per cent of the cases. Venous infarction, often occurring in septic states, is accompanied in many instances by marked toxicity. The kidney is frequently palpable and hematuria is almost always seen.