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Abstract: TH-PO055

Cholemic Tubulopathy as a Cause of AKI: A Cohort Study

Session Information

Category: Acute Kidney Injury

  • 102 AKI: Clinical, Outcomes, and Trials


  • Varghese, Vipin, Ochsner Health, New Orleans, Louisiana, United States
  • Chalmers, Dustin R., Ochsner Health, New Orleans, Louisiana, United States
  • Cohen, Lauren, Ochsner Health, New Orleans, Louisiana, United States
  • Ramanand, Akanksh, Ochsner Health, New Orleans, Louisiana, United States
  • Velez, Juan Carlos Q., Ochsner Health, New Orleans, Louisiana, United States

Cholemic tubulopathy (i.e., bile cast nephropathy) is a type of acute kidney injury (AKI) described in individuals with acute cholestasis (obstructive, drug-induced, infectious, acute alcoholic). However, most of the available evidence comes from isolated case reports. We aimed to describe the clinical characteristics of patients diagnosed with cholemic tubulopathy within a single-center prospective AKI cohort.


We established prospective data collection in patients with AKI stage ≥ 2 (AKIN) over 5-years. Each patient completed microscopic examination of the urinary sediment (MicroExUrSed). The presence of hyaline casts (HC), waxy casts (WxC), renal tubular epithelial cell casts (RTECC), granular casts (GC), and muddy brown granular casts (MBGC) were recorded. We identified patients with documented cholestasis without cirrhosis. Demographic and clinical characteristics were extracted. Cases of shock liver were excluded.


Among 483 patients with AKI without cirrhosis, 22 (4.6%) patients were found to have cholemic tubulopathy as the primary cause of AKI [32% women, 46% white, 27% black, median age 57 (20-84)]. Causes of cholestasis included biliary obstruction due to primary or metastatic cancer (5), biliary stricture (1), drug-induced cholestasis (1), cholelithiasis (6), acute viral hepatitis (3), alcoholic hepatitis (4), and acute liver failure of unknown etiology (2). One case was biopsy-proven bile cast associated acute tubular injury (acute hepatitis A). Median serum bilirubin was 22.8 (5.3-57.7) mg/dL and serum creatinine at presentation was 3.1 (1.4-8.6) mg/dL. By MicrExUrSed, HC, RTECC, GC, MBGC, and WxC were identified 13%, 41%, 64%, 55%, and 28% of patients, respectively.Among patients which had crystals reported, leucine crystals were seen in 5/17 (29%) and bilirubin crystals were seen in 4/17 (24%). Among patients with cholemic tubulopathy, 11 (50%) patients required dialysis, 6 (27%) died, and 6 (27%) recovered kidney function.


Cholemic tubulopathy should be suspected as a cause of AKI in patients with cholestasis with severe hyperbilirrubinemia without an alternative etiology of AKI. Overt evidence of tubular injury is often found by MicrExUrSed.