S2580 Plasmapharesis for Hyperbilirubinemia: A Bridge to Transplant

Abstract

INTRODUCTION: Plasma exchange (PE) has been used to successfully treat hyperbilirubinemia in conditions such as primary biliary cholangitis. However, it is not routinely used to prevent worsening renal function due to bile cast nephropathy, as a bridge to liver transplant. We present a case of using PE to treat severe hyperbilirubinemia in a patient with acute on chronic liver failure prior to orthotopic liver transplantation (OLT). CASE DESCRIPTION/METHODS: This is a 62 year old woman with a past medical of NASH cirrhosis, esophageal varices, hepatic encephalopathy, and factor V leiden deficiency who presented to our institution for management of worsening liver function. On admission, her total bilirubin was 29.3mg/dl (baseline was around 5mg/dl), direct bilirubin 18mg/dl and MELD was 21. Hemolysis workup was negative. She had completed a course of azithromycin for pneumonia, raising concern for drug induced liver injury. MRI abdomen revealed portal vein thrombosis, splenomegaly, portal enteropathy, ascites and no biliary ductal dilation. Her course was complicated by worsening bilirubin up to 70mg/dl and subsequent worsening kidney function with a creatinine of 3.90 mg/dl concerning for cholestatic nephrosis. She was transferred to the intensive care unit where she received two sessions of PE. After PE her bilirubin improved to 40 mg/dl, her creatinine improved to 1.39 mg/dl and urine output improved. Patient was re-MELDed at 40. She successfully underwent OLT ten days after her last PE session. Post-OLT, her bilirubin and creatinine normalized. DISCUSSION: While we are transplanting at higher MELD scores, we see patients with severe hyperbilirubinemia, which can cause significant complications, including bile cast nephropathy. Cholemic nephrosis can cause renal injury from proximal tubulopathy to intrarenal bile cast formation. PE has been used to successfully treat hyperbilirubinemia in few cases of fulminant hepatic failure not amendable to OLT in an attempt to allow hepatocyte recovery and regeneration. However, it is not routinely used to treat hyperbilirubinemia in liver failure as a bridge to transplant. Preserving renal function is important for a successful post-transplant course. Our case is one of the few cases in the literature where PE was used as a bridge prior to OLT in patients with hyperbilirubinemia in the setting of acute on chronic liver failure. Hence we conclude that PE can be considered to treat hyperbilirubinemia to prevent renal failure as a bridge to transplant.