Abstract: SA-PO0378
Dialysis Challenges in a Patient with AKI with Anaplasmosis-Associated Hemophagocytic Lymphohistiocytosis
Session Information
- AKI: Case Reports - Drug/Toxin Injury, Crystals, Obstruction, and Unusual Presentations
October 24, 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
- Rjob, Ashraf S., The Ohio State University Wexner Medical Center, Columbus, Ohio, United States
- Lehmann, Parker, Henry Ford Genesys Hospital, Grand Blanc, Michigan, United States
- Bhatt, Udayan Y., The Ohio State University Wexner Medical Center, Columbus, Ohio, United States
- Thakkar, Asish, Chalmers P. Wylie Veterans Outpatient Clinic, Columbus, Ohio, United States
Introduction
Hemophagocytic lymphohistiocytosis (HLH) is characterized by uncontrolled inflammatory responses that induce multiorgan failure. HLH can be classified as primary or secondary. Acute kidney injury (AKI) in HLH can be > 60%. The etiology of AKI is typically multifactorial. We present a case demonstrating the challenges of renal replacement therapy (RRT) in patients with HLH.
Case Description
A 78yo male presented with recent body aches, fever, and diarrhea. The patient met criteria for sepsis and was noted to have AKI. Antibiotics and testing for sources of infection were initiated. Because of worsening AKI, the patient was started on intermittent hemodialysis (HD). The patient had an elevated creatine kinase (CK), hypertriglyceridemia, elevated transaminases, anemia, thrombocytopenia, and a ferritin level of > 12,000ng/mL. He met multiple criteria for HLH and was started on corticosteroids. His clinical situation deteriorated, however, and he was transferred to our institution.
The patient remained on empiric antibiotics and corticosteroid therapy. An EGD (done for a drop in hemoglobin - Hgb) showed a bleeding duodenal ulcer that was treated. He continued intermittent HD. Ferritin levels improved to about 600ng/mL. PCR testing showed anaplasma viremia, which was thought to have triggered HLH.
The patient developed significant azotemia and hyperphosphatemia but stable potassium levels and Hgb, indicating an increase in inflamation. His ferritin climbed to 947ng/mL. The patient began daily HD. He experienced another drop in Hgb but an EGD and angiogram did not demonstrate active bleeding. The patient exhibited progressive hypotension, hyperkalemia despite daily HD, and anemia. He was transferred to the ICU. His ferritin had improved but was started on CRRT for hyperkalemia. His ferritin then abruptly rose to 39,291ng/mL. Because of progressive deterioration, the patient was transitioned to comfort care and expired.
Discussion
HLH is characterized by uncontrolled inflammation. A variability in systemic inflammation can be expected. Given the high incidence of AKI associated with HLH, the variability in inflammation can manifest with variability in metabolic dysregulation. Our case highlights the fact that deterioration in metabolic or inflammatory parameters should lead to earlier transitions to more continuous forms of RRT, such as CRRT or PIRRT.
Acknowledgment
Ms. Sydney Lehmann for help with proofreading and editing.