Abstract
A 79-year-old woman experienced cardioembolic cerebral infarction in the left cerebral hemisphere. She was treated with the free-radical scavenging agent, Edaravone, without anticoagulant agent because of hemorrhagic changes in the area of infarction. On the 6th day after admission, the serum lactate dehydrogenase (LDH), transaminases and C-reactive protein were markedly elevated. Although the patient she did not complain of low back pain, cast formation of urinary sediment and elevation of LDH isozyme 1 and 2, each suspicious for renal infarction, were detected. Contrast-enhanced abdominal computed tomography and renal scintigraphy demonstrated renal infarction on the left side. Edaravone has been inferred to be a causal agent of acute renal failure. However, some case reports have shown renal infarction to be a cause of acute renal failure during Edaravone treatment. Renal infarction was found not to be unusual among cases with atrial fibrillation and cerebral embolism. It is necessary therefore that cases with an obvious nephrotoxic factor other than Edaravone, such as renal infarction, during Edaravone treatment should be eliminated in order to assess closely the mechanism of acute renal failure caused by Edaravone.
