Kidney Week

Abstract: TH-PO090

A 20-Year-Old Woman Presenting with Hemoptysis Most Likely Caused by H1N1 Influenza-Induced Thrombotic Microangiopathy

Session Information

• AKI: Clinical, Outcomes, and Trials - Epidemiology and Pathophysiology
  October 24, 2024 | Location: Exhibit Hall, Convention Center
  Abstract Time: 10:00 AM - 12:00 PM

Category: Acute Kidney Injury

• 102 AKI: Clinical, Outcomes, and Trials

Authors

• Pal, Aman, Albany Medical Center, Albany, New York, United States

Aman Pal, MD, MBChB

• Aydin-Ghormoz, Emmanuel Albert, Albany Medical Center, Albany, New York, United States

Emmanuel Albert Aydin-Ghormoz, MD

• Mehta, Swati, Albany Medical Center, Albany, New York, United States

Swati Mehta, MD, MBBS, FASN

• Hajianpour, Mj, Albany Medical Center, Albany, New York, United States

Mj Hajianpour, MD, PhD

• Hongalgi, Krishnakumar D., Albany Medical Center, Albany, New York, United States

Krishnakumar D. Hongalgi, MD

Introduction

Thrombotic Microangiopathy (TMA) is a pathological description which clinically presents with thrombocytopenia, microangiopathic hemolytic anemia, and organ dysfunction. The etiology of TMA is broadly classified into four categories: primary hereditary, primary acquired, secondary and infection associated. H1N1 influenza is a rare etiology of complement mediated TMA (CM-TMA) with there being under 30 cases reported to date, and its presentation with hemoptysis makes it a challenging diagnosis.

Case Description

A Caucasian female in her 20s presented to the hospital with a viral prodrome in setting of a new AKI (creatinine 8.2mg/dL), thrombocytopenia (platelet count 14,000/mm³), and H1N1 influenza positive. She developed hemoptysis the next day, with no respiratory distress. Serology for antineutrophilic cytoplasmic antibodies, anti-glomerular basement membrane, and antiphospholipid antibodies were negative. CT chest was also negative for pulmonary hemorrhage. Plasma exchange was commenced until ADAMTS13 activity returned normal. The patient was further commenced on eculizumab after an aHUS/TMA/C3G gene panel was sent. She was found to have splice site variant of MCP/CD46, which was reiterated on a renal biopsy. The genetic results were relayed, including predisposition to future events and the importance of long-term eculizumab treatment.

Discussion

CM-TMA is a consequence of alternative pathway dysregulation with genetic mutations being far more prevalent than acquired antibodies. This dysregulation is generally not causative, rather predisposes affected individuals to CM-TMA. A proposed mechanism that can unmask these latent deficits include infections, such as Influenza virus. Its pathophysiology is thought to be related to the production of neuraminidase (NA), which results in platelet aggregation and endothelial injury. Our case highlights the importance of keeping a broad differential beyond classic pulmonary-renal syndromes in patients presenting with hemoptysis and TMA, while understanding the pathophysiology of infections unmasking genetic mutations in CM-TMA.