Abstract: FR-PO042
COVID-19 Mimicking Classic Hemolytic Syndrome in a Toddler
Session Information
- COVID-19: AKI Outcomes, Biomarkers, Treatments, Case Reports
November 04, 2022 | Location: Exhibit Hall, Orange County Convention Center‚ West Building
Abstract Time: 10:00 AM - 12:00 PM
Category: Coronavirus (COVID-19)
- 000 Coronavirus (COVID-19)
Authors
- Jagadish, Apoorva, LSU Health Shreveport, Shreveport, Louisiana, United States
- Pichilingue Reto, Patricia, LSU Health Shreveport, Shreveport, Louisiana, United States
- Baliga, Radhakrishna, LSU Health Shreveport, Shreveport, Louisiana, United States
Introduction
Coronavirus disease 2019 (COVID-19) is a heterogenous, predominantly pulmonary disease, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Thrombotic microangiopathy (TMA), a triad of hemolytic anemia, thrombocytopenia and end organ damage, is present in severe COVID-19 and Hemolytic uremic syndrome (HUS). Classic HUS is commonly caused by Shiga toxin (ST) producing Escherichia coli 0157:H7 (ST-HUS). We report a toddler with features of classic HUS with positive PCR testing for SARS-CoV-2.
Case Description
A 2-year healthy girl presented with diarrhea of 7 days that turned bloody 2 days prior to admission. Previously, several family members with respiratory symptoms tested positive for COVID-19. On admission, she appeared jaundiced with generalized swelling, BP was 137/85 mm Hg (>99%). By day 2, her diarrhea subsided, she was oliguric, fatigued and listless. She was treated symptomatically and BP was controlled with labetalol. Pertinent laboratory data: Hemoglobin 5.1g/dL, reticulocyte 8.4%, platelets 51 K/μL lactate dehydrogenase 833 U/L and haptoglobin < 8 mg/dl. Serum creatinine (SCr) was 0.71 mg/dl with eGFR of 67 ml/min/1.73m2 and Urine showed +3 protein and blood. Random sample (RS) urine protein to Cr ratio was 5.1 (<0.2). Stool culture was negative for E. coli 0157:H7 and other enteropathogens. Shiga toxin 1 and 2 were negative by enzyme immune assay. Nasal swab was positive for SARS-CoV-2 by PCR. Genetic renal panel v8 for aHUS was negative. Complement, Coombs and ANA negative. ADAMSTS13 level >100%. By day 5, symptoms subsided and kidney function improved significantly with SCr at 0.55 mg/dl (eGFR 81ml/min/1.73m2). She was discharged on Lisinopril. Four months later, BP was 107/73 mm Hg and SCr 0.32 mg/dl (eGFR 127ml/min/1.73m2). Urine had trace protein with RS urine protein to Cr ratio of 0.32.
Discussion
Both COVID-19 and HUS cause severe endothelial dysfunction resulting in release of inflammatory cytokines, complement dysregulation, and development of TMA. COVID-19 has been reported as a potential trigger of aHUS in patients with kidney involvement wherein genetic testing revealed complement defect. Our patient had features of classic HUS, was negative for ST-HUS and ST, but positive for SARS-CoV-2. COVID-19 may be considered in children with bloody diarrhea followed by hemolytic anemia, thrombocytopenia and acute kidney injury.