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Kidney Week

Abstract: TH-PO0774

A Perplexing Case of Bile Cast Nephropathy

Session Information

Category: Acute Kidney Injury

  • 102 AKI: Clinical, Outcomes, and Trials

Authors

  • Brown, Ashlyn, Mayo Clinic Arizona, Scottsdale, Arizona, United States
  • Anvari, Evamaria, Mayo Clinic Arizona, Scottsdale, Arizona, United States
Introduction

Bilirubin can damage renal tubules through multiple pathways by inducing inflammation, blocking tubular flow, causing toxic injury and by impacting vascular supply. This condition should be considered in patients with concurrent renal and liver failure complicated by hyperbilirubinemia.

Case Description

A 62-year-old male with a medical history significant for hypertension, hyperlipidemia, type 2 diabetes, and coronary artery disease presented with liver failure and associated acute renal failure with a total bilirubin peak of 64.5 mg/dL and a creatinine peak of 5.42 mg/dL. Due to associated metabolic complications, patient briefly required renal replacement therapy. Liver biopsy showed cholestatic hepatitis with ductopenia, thought to be secondary to supplement induced vanishing duct syndrome. Kidney biopsy demonstrated evidence of bile cast nephropathy with only 10% interstitial fibrosis and tubular atrophy. Plasma exchange was initiated empirically with significant improvement in renal function and creatinine is now maintained around 0.7-1.0 mg/dL with ongoing plasma exchange therapy to manage hyperbilirubinemia while awaiting definitive treatment with liver transplantation.

Discussion

Management strategies for bile cast nephropathy focus on resolving the underlying pathology contributing to elevated bilirubin levels when possible. Plasma exchange has been employed in similar cases but there are no established protocols in place to guide clinicians. At our institution, recommendations regarding plasma exchange duration and goals for bilirubin maintenance are determined by the department of transfusion medicine.

Bilirubin Casts on Renal Pathology