Abstract: PUB644
Coexistence of Triple Viral Infection as a Trigger of Severe Rhabdomyolysis-Associated AKI in an Adolescent
Session Information
Category: Trainee Case Report
- 1700 Pediatric Nephrology
Authors
- Plotskaya, Natalia, Drexel University College of Medicine, Philadelphia, Pennsylvania, United States
- Mejia, Christina Irene, Drexel University College of Medicine, Philadelphia, Pennsylvania, United States
- Boyle, Suzanne, Drexel University College of Medicine, Philadelphia, Pennsylvania, United States
- Ajelero, Olawunmi, Drexel University College of Medicine, Philadelphia, Pennsylvania, United States
- Soundararajan, Suganthi, Drexel University College of Medicine, Philadelphia, Pennsylvania, United States
Introduction
Rhabdomyolysis has many triggers, including trauma, drugs, autoimmune disorders, infection and genetic mutations. Prevalence of viral-induced rhabdomyolysis is 38% in pediatric population. Here we describe a case of acute kidney injury (AKI) from rhabdomyolysis secondary to viral infection.
Case Description
An 18-year-old African American female college student with past medical history of febrile seizures, Kawasaki disease and obesity presented with a one-week history of myalgias, productive cough, abdominal pain and dark urine. She denied sick contacts, recent travel, rash, arthralgias, trauma. Physical examination revealed tachycardia, abdominal and lower extremities tenderness, inability to ambulate. On admission, creatinine (cr) was elevated at 1.56 mg/dl; potassium, 5 mmol/l; CK>200,000 IU/L, AST, 2033 U/L;ALT, 595 U/L. Urinalysis showed amber urine, 3+ blood, 2+ protein, 1-5 RBC and no casts. Drug screen was negative. Viral and bacterial serologies were negative with the exception of PCR-positive Parainfluenza and Epstein Barr virus (EBV), and Coxsackievirus group B antibodies (titer 1:32). Complement levels were normal, pANCA and cANCA <1:20. ANA titer was 1:160 with speckled pattern. On day 3, lower extremities MRI showed diffuse, symmetric muscle edema. Muscle biopsy demonstrated acute myonecrosis. PCR of muscle sample for EBV was negative. Stains for mitochondrial, glycogen, lipid storage myopathies were unremarkable. The patient was managed with intravenous volume resuscitation. On day 4, cr decreased to 1.25 mg/dl and CK decreased to 183,600 IU/L. On day 14, she was discharged home with normal renal function and CK of 617 IU/L.
Discussion
Coexistence of viral infections led to severe rhabdomyolysis in our patient. However, given the reported history of vasculitis, investigation of potential autoimmune etiology was pursued, and subsequently excluded. As a result, steroid therapy was withheld and resolution occurred with intravenous volume resuscitation alone. Clinicians should have a high index of suspicion for rhabdomyolysis in patients who present with muscle pain and weakness and elevated creatine. Further, timely investigation of the etiology of rhabdomyolysis, including viral, autoimmune, and genetic disorders, has implications for management and prognosis of AKI.