Eculizumab treatment for renal failure in a pediatric patient with COVID-19
- PDF / 609,403 Bytes
- 4 Pages / 595.276 x 790.866 pts Page_size
- 15 Downloads / 165 Views
CASE REPORT
Eculizumab treatment for renal failure in a pediatric patient with COVID‑19 Ruchi Mahajan1 · Marissa Lipton1 · Larisa Broglie2 · Namrata Gargee Jain1 · Natalie Somera Uy1 Received: 19 June 2020 / Accepted: 3 September 2020 © Italian Society of Nephrology 2020
Abstract While there are increasing reports of acute kidney injury among hospitalized adults with COVID-19, there is still limited information on renal complications associated with COVID-19 in children. The cause of kidney involvement in COVID19 is likely multifactorial, and appears to involve a complex process, including complement dysregulation and thrombotic microangiopathy. We present a pediatric case of COVID-19 and renal failure due to thombotic microangiopathy, successfully treated with eculizumab.
Introduction
Case presentation
The number of adults affected by COVID-19 overwhelmingly exceeds pediatric patients, and therefore, the vast majority of studies on renal involvement in COVID-19 have been performed in adults. The incidence and etiology of acute kidney injury (AKI) amongst pediatric patients remains largely unknown. Complement activation has been postulated to underlie some pathophysiology of disease in COVID-19 infections, including thrombotic microangiopathy (TMA). To our knowledge, we present the first pediatric case of COVID-19 and severe AKI due to TMA, treated with eculizumab.
We present the case of a 14 year old female with obesity and asthma, who was admitted to the Pediatric Intensive Care Unit with fever for 7 days, and complaints of abdominal pain, diarrhea, vomiting, myalgias, and chest pain. On admission, she was febrile, tachypneic, and tachycardic, but normotensive. Initial SARS-CoV-2 PCR was negative. On hospital day 2, she became hypotensive, requiring pressor support, and had worsening respiratory distress with oxygen desaturation, requiring intubation. Repeated SARS COV-2 PCR was indeterminate, and antibody testing (IgG) was positive. Laboratory results demonstrated elevated inflammatory markers, with ferritin > 100,000 ng/mL, CRP > 300 mg/dL, and WBC 33,000/µL. Serum creatinine (Cr) on admission was 0.7 mg/dL (eGFR 85 mL/min/1.73 m 2 by modified Schwartz formula), but she developed oliguric AKI on hospital day 3, and her peak Cr was 8.97 mg/dL on hospital day 7. Although she was responsive to diuretic treatment with moderate increase in urine output, she developed progressive fluid overload with worsening uremia (BUN 170 mg/dL) and metabolic acidosis. Urinalyses demonstrated 100–300 mg/ dL protein with moderate-large blood, with variable RBCs (ranging from 2 to 59/hpf). Creatine kinase (CK) (55,695 U/L, normal 40–308 U/L) and urine myoglobin (102 mg/L; normal 0–1 mg/L) were elevated, suggestive of viral-induced rhabdomyolysis, also contributing to AKI, but CK downtrended as creatinine worsened. She also had mild thrombocytopenia (platelets 126,000/ mL) and hemolytic anemia (nadir Hgb 6.8 g/dL), requiring
Ruchi Mahajan and Marissa Lipton: co-lead authors, equal contributions. * Natalie Somera Uy nsu1@cu
Data Loading...
