Abstract: SA-PO0107
The Bilirubin Blues: Plasma Exchange for Bilirubin Nephropathy
Session Information
- AKI: Clinical Diagnostics and Biomarkers
November 08, 2025 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Acute Kidney Injury
- 102 AKI: Clinical, Outcomes, and Trials
Authors
- Lurie, Andrew, Lakeland Regional Health Medical Center, Lakeland, Florida, United States
- Luna, Graciela M., Lakeland Regional Health Medical Center, Lakeland, Florida, United States
- Trube, Jennifer, Lakeland Regional Health Medical Center, Lakeland, Florida, United States
- Rodriguez Padilla, Juan O, Lakeland Regional Health Medical Center, Lakeland, Florida, United States
- Ahmed, Umair S., Lakeland Regional Health Medical Center, Lakeland, Florida, United States
- Sherieh, Assem, Lakeland Regional Health Medical Center, Lakeland, Florida, United States
Introduction
Bilirubin or cholemic nephropathy is a rare but serious complication of severe hyperbilirubinemia. It is characterized by acute kidney injury (AKI) caused by bilirubin-induced tubular toxicity. While supportive care is the standard treatment, therapeutic plasma exchange (TPE) has emerged as a potential intervention to reduce bilirubin levels and improve renal outcomes.
Case Description
A 28-year-old male with a history of alcohol abuse and a recent admission for acute alcoholic hepatitis presented with worsening abdominal pain. He was being evaluated for transfer to a liver transplant center. On admission, laboratory testing revealed a creatinine of 15 mg/dL and total bilirubin of 20 mg/dL. He had previously failed to respond to Terlipressin for presumed hepatorenal syndrome. Due to worsening renal function, hemodialysis was initiated. Given the strong clinical suspicion for bilirubin nephropathy as the cause of AKI, TPE was initiated.
The patient underwent 3 sessions of TPE, which led to marked improvement in both renal and hepatic function.
Discussion
TPE is an extracorporeal therapy that removes large molecular weight substances, such as bilirubin, from the bloodstream. While it remains experimental in the setting of bilirubin nephropathy, it may be beneficial in cases of severe hyperbilirubinemia associated AKI that are resistant to conventional therapies.
This case highlights the importance of considering bilirubin nephropathy in patients with liver dysfunction and unexplained AKI. Though not yet standard of care, TPE may offer a promising therapeutic option for improving renal outcomes by rapidly reducing toxic bilirubin levels.
Comprehensive Metabolic Panel
| Laboratory | Admission | Discharge |
| BUN | 156 mg/dL | 23 mg/dL |
| Creatinine | 15 mg/dL | 1.16 mg/dL |
| Sodium | 130 mEq/L | 145 mEq/L |
| Potassium | 4.2 mEq/L | 4.3 mEq/L |
| Chloride | 93 mEq/L | 108 mEq/L |
| CO2 | 15 mEq/L | 24 mEq/L |
| Anion Gap | 28 mEq/L | 13 mEq/L |
| Albumin | 3.86 g/dL | 3.90 g/dL |
| Total Bilirubin | 20 mg/dL | 4.6 mg/dL |
| Alkaline Phosphatase | 199 U/L | 235 U/L |
| Aspartate aminotransferase | 114 U/L | 102 U/L |
| Alanine aminotransferase | 771 U/L | 253 U/L |