Abstract: SA-PO0047
Bulging Biceps with Brugada Syndrome: Unexpected Cause of AKI Following Sudden Cardiac Arrest
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
- Ahmed, Taha, Houston Methodist Hospital, Houston, Texas, United States
- Farooqui, Ozer A., Houston Methodist Hospital, Houston, Texas, United States
- Olivero, Juan Jorge, Houston Methodist Hospital, Houston, Texas, United States
- Adrogue, Horacio E., Houston Methodist Hospital, Houston, Texas, United States
- Edwards, Angelina, Houston Methodist Hospital, Houston, Texas, United States
Introduction
Brugada Syndrome is a rare genetic disorder marked by life-threatening ventricular tachyarrhythmias and sudden cardiac arrest. Often asymptomatic and undiagnosed, tachyarrhythmias are provoked by medications or autonomic dysfunction. We present a case of Brugada syndrome-associated ventricular fibrillation cardiac arrest with multi-factorial acute kidney injury (AKI) initially attributed to cardiorenal syndrome type 1, with later development of rhabdomyolysis-induced AKI and ischemia-reperfusion-induced AKI in a muscular man undergoing elective surgery.
Case Description
A 47-year-old muscular male with a past medical history of hyperlipidemia, hypogonadism on testosterone replacement, exercised-induced rhabdomyolysis presented for elective cervical fusion for chronic radiculopathy. Following anesthesia induction, telemetry revealed ventricular tachycardia which evolved into ventricular fibrillation. Acute Cardiac Life Support was initiated with return of spontaneous circulation after three defibrillator shocks. Within 24 hours, labs showed stage 2 AKI (baseline creatinine 1.4 mg/dL to 3.08 mg/dL) and subsequent stage 3 AKI (peak 4.46 mg/dL). Creatinine kinase was greater than 55,000 U/L and urine was brown, turbid and positive for myoglobin. Muscle break-down was attributed to electrical shocks in the setting of large muscle mass. Both oral and IV hydration were encouraged with gradual resolution of the AKI without renal replacement therapy over twenty days. Review of historic EKGs showed ST elevations in V1 and V2 of Brugada type III and a current procainamide challenge was positive for inducible type I Brugada. An AICD was placed to prevent future sudden cardiac death.
Discussion
This case underscores the renal impact of unforeseen cardiac arrest in Brugada Syndrome, particularly during anesthesia induction. Abnormal depolarization of cardiac myocytes, arrhythmia and sudden hemodynamic collapse precipitated cardiorenal syndrome type 1. Additionally, electrical defibrillator shocks in a patient with large muscle mass led to rhabdomyolysis-associated AKI. Upon restoration of spontaneous circulation, reperfusion-injury further potentiated the patient’s kidney injury. Careful consideration of past EKGs and a heightened index of suspicion are key for diagnosis and management.