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Sudden cardiac death in nephrology: focus on acquired long QT syndrome.

More than a half million Americans have end-stage renal diseases (ESRD), 20 millions have been diagnosed with chronic kidney disease (CKD) and another 20 millions are individuals at risk [1]. The ESRD patients population is characterized as one with the highest mortality rate (even when adjusted for age, race, sex and comorbid conditions), comparable with patients in advanced stages of breast cancer [2]. Among dialysis patients in the United States, cardiovascular disease (CVD) mortality is 30 times higher than in general population and accounts for 58% of all-cause mortality, and the risk for arrhythmogenic death is one of the highest among any other populations [3]. The situation is greatly exacerbated by the fact that there is a clinically proven lack of benefits from: (a) implantable cardioverter-defibrillators in patients with severe renal disease and heart failure [4], and (b) the statins on the risk of cardiovascular events in the advanced CKD [5]. This presents the questions: why are renal patients so vulnerable to fatal arrhythmias and what else can be done to prevent sudden cardiac death (SCD) in this population? The main goal of this review is to bring to the attention of the nephrology community some of the latest developments in the field of experimental and clinical cardiac electrophysiology and the pharmacology of SCD. A special focus is placed on the molecular, ionic and pharmacological aspects of acquired long QT syndrome (LQTS), its clinical manifestation and prevention. Acquired long QT syndrome in nephrology