Abstract: FR-PO0441
Thrombotic Microangiopathy Secondary to Pancreatitis: A Rare but Recognized Cause
Session Information
- AKI: Case Reports - TMA, Vasculitis, Immune-Mediated Injury, and Systemic Disease
October 23, 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
- Millet, Leandre Michael, LSU Health New Orleans, New Orleans, Louisiana, United States
- Mohandas, Rajesh, LSU Health New Orleans, New Orleans, Louisiana, United States
- Bajracharya, Siddhartha Darshan, LSU Health New Orleans, New Orleans, Louisiana, United States
Introduction
Thrombotic Microangiopathy (TMA) is a clinical syndrome characterized by the triad of hemolytic anemia, thrombocytopenia, and acute kidney injury. Early diagnosis and treatment are critical to reducing associated morbidity and mortality. We present a case of secondary TMA in a 37-year-old patient with pancreatitis.
Case Description
A 37-year-old female with a past medical history of type 2 diabetes mellitus and hypertension presented to the emergency room with a one day history of right, upper abdominal pain. They denied any prior episodes or significant family history. They smoked three tobacco cigarettes daily and drank a fifth of vodka daily. On admission, notable findings included a lipase of 954 U/L, triglycerides of 1930 mg/dL, and CT imaging of the abdomen consistent with acute pancreatitis. The patient was started on an insulin drip for her elevated blood triglycerides. By hospital day four, the patient’s creatinine had risen to 4.9 mg/dL from a baseline of 0.6 mg/dL, their hemoglobin dropped to 9.3 gm/dL, and their platelet count decreased to 54,000. Other significant labs included a haptoglobin of <30 mg/dL, an LDH of 1593 U/L, an ADAMTS 13 activity of 77.1 %, and a negative Shiga-toxin. Their peripheral smear showed a decreased platelet count and anisopoikilocytosis. An aHUS genetic panel revealed a heterozygous missense variant of uncertain significance on the MASP2 gene. The laboratory abnormalities were concerning for a TMA, possibly atypical hemolytic uremic syndrome (aHUS). Renal biopsy was deferred because the ICU team felt the patient was medically unstable for the procedure. Empiric eculizumab therapy was considered but never instituted. However, by hospital day six, the patient's creatinine and urinary output began to improve, and they never required kidney replacement therapy. Seven months later the creatinine and hemoglobin were both back to within the normal reference ranges.
Discussion
Pancreatitis is a known but uncommon cause of secondary TMA and can mimic aHUS. The distinction is critical as early treatment with eculizumab is warranted for aHUS. Genetic testing results are rarely available in time to guide therapy and often inconclusive. The spontaneous recovery of renal function and hemolysis in our patient argues for a secondary TMA from pancreatitis. The MASP2 VUS should be interpreted cautiously, as elevated MASP2 levels have been observed across multiple TMA subtypes.