A 35-year-old male visited the emergency department with symptoms of nausea, abdominal discomfort, and oliguria. These symptoms and signs developed abruptly several days prior to visit, so he took a digestive medicine, however, these symptoms aggravated. He had no signs of diabetes or chronic hepatitis. His skin color was yellowish on physical examination. His vital signs were stable on arrival. However, serum total bilirubin, direct bilirubin, and creatinine were 10.29 mg/dL, 7.95 mg/dL, and 14.30 mg/dL respectively. Immunoglobulin M, the antibody for acute hepatitis A, showed positive results, however, anti-neutrophil cytoplasmic antibodies and complements were all within normal range. His uremic symptoms aggravated despite aggressive fluid therapy. His general condition improved partially after hemodialysis, however, several clinical signs still remained during the next four weeks. He underwent a renal biopsy. The pathologic result showed that the renal tubular lumens frequently contained dark pigment casts with foreign body reactions and calcification, and interstitium focally exhibited mononuclear cell infiltration and fibrosis (Fig. 1).

Bile casts can result in acute kidney injury of patients with severe jaundice and hepatic failure. Further, a direct bilirubin toxicity for renal tubules may also contribute to this renal injury. This case suggests that recovery of acute tubular necrosis can be delayed by the presence the tubular bile cast.