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Abstract: TH-PO673

Thrombotic Microangiopathy Secondary to Acute Pancreatitis: A Rare Association

Session Information

Category: Glomerular Diseases

  • 1402 Glomerular Diseases: Clinical, Outcomes, and Trials

Authors

  • Tomar, Ojaswi Singh, Washington University in St Louis, St Louis, Missouri, United States
  • Java, Anuja, Washington University in St Louis, St Louis, Missouri, United States
Introduction

Thrombotic microangiopathy (TMA) due to acute pancreatitis is rare with only 35 cases reported since 1978. The diagnosis requires a high index of suspicion and if not managed timely, can lead to severe morbidity and mortality. Here we report a case of TMA due to acute pancreatitis that was promptly recognized and successfully treated with Eculizumab.

Case Description

A 58-yo woman presented with one-day history of abdominal pain, nausea and vomiting after ingesting seafood. She was Jehovah’s witness. Labs on admission showed an elevated lipase, 1900 U/L (13-60 U/L). Serum creatinine was at baseline (1.7 mg/dl). Treatment for acute pancreatitis was initiated. Two days later, serum creatinine increased to 8 mg/dl. Labs also showed features of microangiopathic hemolytic anemia and thrombocytopenia (Hgb 4 g/dl, platelet 46 K/uL, haptoglobin < 10 mg/dl, lactate dehydrogenase 2424 U/L). Schistocytes (>10/hpf) were present on peripheral smear. ADAMTS13 activity was normal. C3 was low normal at 99 mg/dl (normal range, 90-180 mg/dl) and C4 was normal. TMA was suspected and eculizumab started on day 7. Two days after starting eculizumab, platelet count improved to 128 K/uL, hemoglobin to 7 g/dl, LDH was 800 U/l and haptoglobin normalized. She remained dialysis dependent on discharge but 4 weeks later renal function recovered and she came off dialysis. Serum creatinine 6 weeks later is 3.6mg/dl. She remains on eculizumab. Genetic testing did not show any pathogenic mutations.

Discussion

Pancreatitis can occur in 2% of cases due to TMA, but pancreatitis causing TMA is exceedingly rare. In cases where TMA causes acute pancreatitis, it precedes the onset of pancreatitis, whereas, when acute pancreatitis causes TMA, it manifests typically 2-3 days after the pancreatitis (as in our case). The etiology of TMA after pancreatitis is speculated to be due to inflammatory mediators causing vascular endothelial injury, transient complement activation and ADAMTS13 inhibition. Eculizumab has been shown to shorten renal and hematological recovery but only reported in 3 of 35 cases. Most patients can stop the drug after 3-6 months. Importantly, in our case, we treated with eculizumab since she was Jehovah’s witness and refused plasma exchange. AKI in acute pancreatitis can have a broad differential but early recognition of TMA-induced AKI can be lifesaving.