Abstract: SA-PO0057
Diarrhea-Negative Hemolytic Uremic Syndrome Due to Norovirus Infection
Session Information
- AKI: Novel Patient Populations and Case Reports
November 08, 2025 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Acute Kidney Injury
- 101 AKI: Epidemiology, Risk Factors, and Prevention
Authors
- Stickles, Eric Benjamin, Lincoln Memorial University - Knoxville Site, Knoxville, Tennessee, United States
- Walden, Lindsay B, Lincoln Memorial University - Knoxville Site, Knoxville, Tennessee, United States
- Papazian, Wendy, East Tennessee Children's Hospital, Knoxville, Tennessee, United States
- Subtirelu, Mihail, East Tennessee Children's Hospital, Knoxville, Tennessee, United States
- Mannemuddhu, Sai Sudha, East Tennessee Children's Hospital, Knoxville, Tennessee, United States
Group or Team Name
- ETCH Nephrology.
Introduction
Hemolytic Uremic Syndrome (HUS) is the most common cause of acute renal failure in children. We report a case of a child with diarrhea negative HUS, not explained by traditional typical or atypical etiologies.
Case Description
A previously healthy 5-year-old boy presented with jaundice and dark colored urine for 1 day. His illness started a week prior with fever for a day, abdominal pain and vomiting for 3 days without diarrhea. Parteint was tachycardic (heart rate 104 bpm) with otherwise stable vital signs. Laboratory evaluation (Table 1) revealed acute kidney injury (creatinine 3.01 mg/dL, BUN 133.8 mg/dL), metabolic acidosis, normocytic anemia without schistocytes, and thrombocytopenia. Low albumin ,hyperuricemia, high phosphorus and LDH. Serum complement levels were normal. Urinalysis showed trace ketones, blood (5–9 RBC/hpf), and pyuria (10–24 WBC/hpf). He received NS bolus and was admitted to the hospital. Due to persistent renal failure acute hemodialysis (HD) was initiated. He needed 4 sessions of HD. He received lisinopril for hypertension and packed red cells and platelet transfusions. Polymerase chain reaction testing for Shiga toxin-producing Escherichia coli was negative but stool testing was positive for norovirus. Functional complement assay including ADAMTS13 was normal. Patient was discharged home after 10 days of hospitalization on Lisinopril. Genetic testing showed heterozygous deletion (AR) of CFHR3-CFHR1 and two polymorphic variants in the C5 genes. At 4 months follow up, his clinical and laboratory parameters normalized.
Discussion
In the absence of genetic mutations, patients with HUS due to norovirus should have complete recovery as seen in our patient and other small number of case reports. This case underscores the importance of considering nontraditional emerging infectious triggers, such as norovirus, in patients with HUS and negative conventional serologic and genetic testing.