Kidney Week

Abstract: SA-PO0195

Rotavirus-Triggered Complement-Mediated Atypical Hemolytic Uremic Syndrome in an Adult

Session Information

• Tubular, Metabolic, and Systemic Noncystic Genetic Kidney Diseases
  October 24, 2026 | Location: Exhibit Hall A, Convention Center
  Abstract Time: 10:00 AM - 12:00 PM

Category: Genetic Diseases of the Kidneys

• 1202 Genetic Diseases of the Kidneys: Non-Cystic (Complex and Non-Cystic Monogenic)

Authors

• Zaidi, Minhal, Houston Methodist, Houston, Texas, United States

Minhal Zaidi, MD

• Khan, Ridwan, Houston Methodist, Houston, Texas, United States

Ridwan Khan, MD

• Thukral, Gauri, Houston Methodist, Houston, Texas, United States

Gauri Thukral, MBBS

• Wiechmann, Catherine, Houston Methodist, Houston, Texas, United States

Catherine Wiechmann, MD

• Narcisse, Victor, Houston Methodist, Houston, Texas, United States

Victor Narcisse, MD

• Rice, Lawrence, Houston Methodist, Houston, Texas, United States

Lawrence Rice, MD

• Das, Dolon C., Houston Methodist, Houston, Texas, United States

Dolon C. Das, MD

• Moreno, Vanessa, Houston Methodist, Houston, Texas, United States

Vanessa Moreno, MD

Introduction

Hemolytic uremic syndrome (HUS) is a thrombotic microangiopathy (TMA) defined by microangiopathic hemolytic anemia, thrombocytopenia, and acute kidney injury. While Shiga-toxin associated-HUS remains the most common etiology, atypical-HUS (aHUS) results from dysregulation of the alternative complement pathway. Infectious triggers, including viral pathogens, have been implicated but are infrequently reported in adults.

Case Description

A 38-year-old male with no past medical history presented with several days of diarrhea, fatigue, and dark urine. On admission, he was found to have severe thrombocytopenia, anemia, reticulocytosis, elevated lactate dehydrogenase, and worsening renal function. Peripheral blood smear showed schistocytes. He had normal ADAMTS13 activity, excluding thrombotic thrombocytopenic purpura. Shiga-toxin testing was negative while stool studies were positive for rotavirus. Given persistent kidney injury, renal biopsy was performed showing chronic active TMA with fibrin microthrombi and glomerular basement membrane remodeling. Electron microscopy revealed concurrent severe podocytopathy. Complement genetic testing identified a rare CD46 variant and factor H mutation, both associated with aHUS. Eculizumab was initiated, with subsequent hematologic recovery and improvement in renal function.

Discussion

This case highlights rotavirus as a potential trigger for complement-mediated aHUS in adults. In patients presenting with TMA and negative evaluation for Shiga toxin and ADAMTS13 deficiency, complement-mediated disease should be considered. Early diagnosis and timely initiation of complement inhibitors are critical to optimizing renal and hematologic outcomes.