Letter to the Editor QT interval prolongation and ventricular fibrillation in childhood end-stage renal disease Gi Beom Kim a , Hee Yeon Cho a , Bo Sang Kwon a , Eun Jung Bae a, ⁎ , Chung Il Noh a , Jung Yeon Choi a , Yong Soo Yun a , Yong Choi a , Jong Won Ha b a Department of Pediatrics, Seoul National University Children's Hospital, 28 Yongon-dong, Chongno-gu, Seoul 110-744, South Korea b Department of General Surgery, Seoul National University Hospital, Seoul 110-744, South Korea Received 29 January 2007; accepted 23 April 2007 Available online 21 August 2008 Abstract Ventricular arrhythmia is a major cause of death in end-stage renal disease (ESRD). Corrected QT (QTc) interval prolongation, which is one of the predictors of ventricular arrhythmia, may be associated with ESRD. We report an 11-year-old boy who had ESRD with marked QTc interval prolongation and developed torsade de pointes with subsequent ventricular fibrillation during the induction of anesthesia. QTc interval was normalized completely after renal transplantation. © 2007 Elsevier Ireland Ltd. All rights reserved. Keywords: End-stage renal disease; Long QT; Torsade de pointes 1. Introduction Ventricular arrhythmia is a major cause of death in end- stage renal disease (ESRD), accounting for 1.4% to 25% of cardiac arrest within 36 months after the onset of ESRD [1]. Corrected QT (QTc) interval prolongation is a predictor of ventricular arrhythmia. Torsade de pointes (TdP) with subsequent ventricular fibrillation (VFi) can be a cause of sudden death in ESRD. We report an 11-year-old boy who had ESRD with prolonged QTc interval and developed VFi secondary to TdP during the induction of anesthesia. 2. Case report An 11-year-old boy presented to the emergency department with a 1-week history of vomiting and diarrhea and a 2-day history of oliguria and dyspnea. He was previously healthy except for proteinuria which was incidentally found 3 years earlier. A family history of sudden death was denied. On physical examination, remote heart sound was audible with grade II/VI holo-systolic murmur at the apex, and breath sound was audible with diffuse rales. He had no weight gain or pitting edema. Biochemical profiles on admission were as follows: BUN, 167 mg/dL; serum creatinine, 11.9 mg/dL; potassium, 4.9 mmol/L; calcium, 3.5 mg/dL (ionized calcium, 0.8 mmol/ L); and estimated glomerular filtration rate, 7 mL/min/1.73 m 2 . Chest radiograph showed cardiomegaly (cardiothoracic ratio, 0.63) with water-bottle shape. Kidney Doppler examination showed bilateral contracted kidneys with poor perfusion. Electrocardiograph on admission showed sinus rhythm with 600 ms of RR interval, 618 ms of QTc interval, and 64 ms of QTc dispersion. Echocardiography showed dilated left ventricle (LV) internal diameter of 52 mm at end-diastole, 21% of LV ejection fraction, moderate mitral regurgitation, mild pericardial effusion, and 122 g/m 2 of LV mass. Under the diagnosis of chronic renal failure of unknown origin, hemodialysis was performed at 1 day after admission. Dobutamine was infused for inotropic support at 3 days after admission. At 4 days after admission, he underwent catheter insertion for persistent hemodialysis. During the induction of anesthesia, he developed TdP with subsequent VFi. Defibril- lation followed by infusing 40 mL of 1% lidocaine and 2 International Journal of Cardiology 127 (2008) e126 – e128 www.elsevier.com/locate/ijcard ⁎ Corresponding author. Tel.: +82 2 2072 3097; fax: +82 2 743 3455. E-mail address: eunjbae@plaza.snu.ac.kr (E.J. Bae). 0167-5273/$ - see front matter © 2007 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2007.04.126