Abstract: TH-PO0773
Therapeutic Plasma Exchange for Bile Cast Nephropathy from Sickle Cell Intrahepatic Cholestasis: A Guideline-Free Indication
Session Information
- AKI: Critical Care, CKRT, Cardiorenal Syndromes, and Clinical Outcomes
October 22, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Acute Kidney Injury
- 102 AKI: Clinical, Outcomes, and Trials
Authors
- Muralidharan, Suchitra, University of Cincinnati, Cincinnati, Ohio, United States
- Pervaze, Shohan, University of Cincinnati, Cincinnati, Ohio, United States
- Andrews, Trisha, University of Cincinnati, Cincinnati, Ohio, United States
- Gudsoorkar, Prakash Shashikant, University of Cincinnati, Cincinnati, Ohio, United States
Introduction
Bile cast nephropathy (BCN) from sickle cell intrahepatic cholestasis (SCIC) is a rare cause of AKI. American Society for Apheresis (ASFA) guidelines do not currently categorize SCIC-induced BCN, leaving therapeutic plasma exchange (TPE) as an unguided rescue therapy. This case explores the durability and cessation criteria for TPE in this setting.
Case Description
A 36-year-old man with homozygous sickle cell anemia (HbSS), hypertrophic cardiomyopathy, and pulmonary hypertension presented with intractable back pain, headache, vomiting, and scleral icterus. Admission labs: total bilirubin >60 mg/dL (RI: 0.2-1.2), lactate dehydrogenase 1,345 U/L (RI: 140-280), haptoglobin <30 mg/dL (RI: 16-200), reticulocytes 17.35% (RI: 0.5-2.5%), and serum creatinine (Cr) 2 mg/dl ( preadmission 0.4 mg/dL). By day 4, Cr peaked at 3.92 mg/dL (RI: 0.7-1.3). Urine microscopy showed yellow-brown bilirubin casts. CT revealed congestive hepatopathy and decreased renal enhancement. We initiated TPE (5 sessions) with fresh-frozen plasma/5% albumin and red cell transfusion (HbS 67% to 22.5%). By day 10, bilirubin declined to 39.9 mg/dL and Cr to 1.6 mg/dL. He was discharged on day 15 (bilirubin 32.3). Without further TPE, bilirubin cleared spontaneously over five months without recurrent AKI. At six months, bilirubin was 10.3, and Cr was ~1.0.
Discussion
TPE successfully bridged the acute hemolytic-cholestatic crisis. Once SCIC was resolved, native clearance pathways managed residual bilirubin without further apheresis. This suggests that for SCIC-induced BCN, clinical stabilization—rather than a fixed bilirubin threshold—may be an appropriate endpoint for TPE cessation.
Hospital Course
| Treatment Day | Preadmission | 0 (Admission) | 2 | 4 | 6 | 8 | 10 | 15 (Discharge) |
| Treatment | None | Initial work up | PLEX initiated | 2 | 3 | 4 | 5 (final session) | None |
| Creatinine | 0.4 mg / dl | 2 mg / dl | 2.79 mg / dl | 3.92 mg / dl | 3.61 mg / dl | 3.09 mg / dl | 2.38 mg / dl | 1.6 mg / dl |
| Total Bilirubin | >60 mg /dl | >60 mg / dl | > 60 mg / dl | >60 mg / dl | 52 mg / dl | 39.9 mg / dl | 32.3 mg /dl |