Abstract: PUB004
Are Bile Casts in AKI Pathogenic? A Potential Role for Therapeutic Plasmapheresis
Session Information
Category: Acute Kidney Injury
- 102 AKI: Clinical, Outcomes, and Trials
Authors
- Ahmad, Sarmad, Rush University Medical Center, Chicago, Illinois, United States
- Whittier, William Luke, Rush University Medical Center, Chicago, Illinois, United States
Introduction
Bile cast nephropathy (BCN) is not often considered in pts with hyperbilirubinemia & acute kidney injury (AKI). Hyperbilirubinemia is often seen in patients with underlying cirrhosis with hypotension who can develop hemodynamic AKI, but bile casts are often seen histopathologically and can be considered incidental. We present a pt with AKI and drug induced liver injury who has isolated hyperbilirubinemia without hemodynamic instability. His kidney biopsy revealed BCN and ATN and his AKI improved with removal of bilirubin by plasmapheresis (PLEX).
Case Description
A 36-y/o man presents with fatigue, pruritus and yellowing of his skin. He has a remote IVDU history, and was taking testosterone, trenbolone, and anavar (held on admission). No NSAIDs or nephrotoxic medications. On exam, his BP was 152/70, HR 72 with icterus & jaundice. He was muscular, with no chronic liver disease sequelae. On admission his serum creatinine was 1.8 mg/dL, total bilirubin 45.5 mg/dL, albumin 2.9 g/dL, AST 29 U/L, ALT 21 U/L, INR 1.17. UA dark, turbid, 4+ bilirubin, no prot/blood, + muddy brown casts. FENa 3.1%. Urine PCR 146 mg/g, urine ACR 33 mg/g. Liver biopsy revealed drug induced liver injurly, attributed to supplements. Renal biopsy demonstrated bile casts and acute tubular injury with minimal fibrosis. His bilirubin and creatinine continued to climb & he was treated with PLEX and HD until renal recovery (Fig 1). His bilirubin levels improved with PLEX and was discharged without any outpatient need for HD or PLEX.
Discussion
Patients with AKI in liver disease and hyperbilirubinemia often exhibit bile casts histologically, with AKI often blamed on ischemia as opposed to bile casts themselves. This case highlights a pt with severe hyperbilirubinemia and AKI without ischemic insults, and on kidney biopsy is found to have bile casts and ATN. This lends support to bile casts potentially having a pathogenic role in AKI. In addition, PLEX is effective at removing bilirubin and its use in our pt may have promoted his renal recovery.