# The Hideous Side of Acute Pancreatitis: A Case of Pancreatitis-Induced Atypical Hemolytic Uremic Syndrome

## TL;DR

A rare case shows acute pancreatitis can cause a severe blood and kidney condition, requiring quick treatment and better diagnostic tools.

## Contribution

Highlights the diagnostic challenges of TMA triggered by acute pancreatitis and advocates for rapid in-house assays.

## Key findings

- Acute pancreatitis can trigger TMA through systemic inflammation and complement activation.
- Empiric plasma exchange and corticosteroids improved the patient's condition despite inconclusive complement studies.
- Delayed ADAMTS13 and complement testing may limit accurate diagnosis, emphasizing the need for rapid assays.

## Abstract

Thrombotic microangiopathy (TMA) is a medical emergency characterized by thrombocytopenia, microangiopathic hemolytic anemia, and acute kidney injury (AKI). Its subtypes, including thrombotic thrombocytopenic purpura (TTP), atypical hemolytic uremic syndrome (aHUS), and secondary TMA, require rapid differentiation due to divergent treatments. Acute pancreatitis, in some cases, can trigger TMA through systemic inflammation and complement activation. A middle-aged male with chronic kidney disease and diabetes was admitted for acute pancreatitis, likely in the setting of glucagon-like peptide-1 (GLP-1) use. On day 3, he developed progressive thrombocytopenia, anemia, and worsening renal function. Peripheral smear showed schistocytes; laboratory values were remarkable for hemolysis. Given the high suspicion for TMA and a PLASMIC score of 5, empiric plasma exchange and corticosteroids were initiated, which showed clinical improvement. ADAMTS13 activity returned at 99%, effectively excluding TTP. Complement studies for aHUS were inconclusive and were obtained post-plasma exchange, which can alter results. The patient completed five sessions of plasma exchange and was discharged in stable condition. A follow-up was arranged for hematology. This case highlights the diagnostic complexity of TMA triggered by acute pancreatitis and the necessity of early empiric treatment. It also calls attention to the limitations of delayed ADAMTS13 and complement testing and advocates for broader implementation of rapid in-house assays to guide timely, precise therapy.