| 초록 |
Case Presentation: A 48-year-old male with no significant past medical history presented to the nephrology department with generalized weakness and oliguria. Upon admission, his laboratory findings were as follows: BUN/Cr 49/10 mg/dL, AST/ALT/T-bil 2349 U/L/3835 U/L/8.78 mg/dL, albumin 3.6 g/dL, PT/INR 10.6 sec/0.94. Abdominal CT showed no abnormalities in hepatobiliary or urinary track, and kidney size was normal. Anti-HAV IgM was positive, confirming a diagnosis of acute hepatitis On the second day of admission, he developed anuria and signs of pulmonary edema, and he underwent emergency hemodialysis. Despite symptomatic treatment, there was no recovery of kidney function, so a renal biopsy was performed on the 6th day of hospitalization to determine the cause of renal failure. The biopsy showed minimal mesangial alteration and tubular obstruction due to bile casts (Figure 1). Starting on the 11th day of hospitalization, the patient began urinating more than 100 mL, and urine output continued to increase. Hemodialysis was stopped on the 19th day of hospitalization, and by the 30th day, his kidney function improved with a Cr of 3.46 mg/dL and liver function with a T-bil of 1.79 mg/dL, and he was discharged (Figure 2). Discussion: Acute hepatitis A typically presents with mild symptoms and improves with symptomatic treatment, but in rare cases, it can lead to acute kidney injury as an extrahepatic complication. The primary causes of renal injury are thought to include hemodynamic changes in the renal arteries due to portal hypertension, viral-induced tubulointerstitial nephritis, and glomerular damage. Recently, bile cast nephropathy, due to biliary sludge in patients with hyperbilirubinemia, has emerged as a potential cause of acute kidney injury. We report a case of bile cast nephropathy complicating acute hepatitis A, which was diagnosed and treated through renal biopsy, along with a review of the literature. |