{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,13]],"date-time":"2026-10-13T20:42:41Z","timestamp":1791924161753,"version":"4.3.4"},"reference-count":78,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2026,8,21]],"date-time":"2026-08-21T00:00:00Z","timestamp":1787270400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2026,8,21]],"date-time":"2026-08-21T00:00:00Z","timestamp":1787270400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J Intern Med"],"published-print":{"date-parts":[[2026,11]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Sudden cardiac death (SCD) is a leading cause of mortality across the chronic kidney disease (CKD) continuum and becomes particularly prominent in dialysis\u2010dependent kidney failure. In hemodialysis, SCD accounts for roughly one quarter to one third of all deaths and up to 60%\u201375% of cardiovascular mortality, with marked temporal clustering around the long interdialytic interval and the first post\u2010interval session. Traditional views have emphasized descriptive epidemiology and presumed ventricular tachyarrhythmias. More recent device\u2010based studies challenge this paradigm, revealing a heterogeneous arrhythmic spectrum in which bradyarrhythmias, pauses, and conduction system disease are often at least as frequent as sustained ventricular tachycardia or fibrillation. This narrative, non\u2010systematic review synthesizes epidemiologic, mechanistic, and interventional data on SCD in CKD and dialysis, with particular emphasis on insights from implantable loop recorder and implantable cardioverter\u2013defibrillator cohorts and on modifiable dialytic and pharmacologic factors. A framework for prevention is proposed around three interacting domains: the structural myocardial substrate, the electrophysiologic milieu, and dialysis\u2010related triggers. Within this framework, contemporary heart failure and CKD therapies (including sodium\u2013glucose cotransporter 2 inhibitors, angiotensin receptor\u2013neprilysin inhibitors, mineralocorticoid receptor antagonists, and beta\u2010blockers), individualized dialysis prescriptions (targeting potassium, calcium, bicarbonate, ultrafiltration, and scheduling), and selective use of device therapy are considered complementary components of mechanism\u2010driven SCD prevention. Methodological challenges in defining and adjudicating SCD in CKD are discussed, and priorities are outlined for improved phenotyping, continuous rhythm monitoring, and CKD\u2010specific risk stratification, with the overarching aim of moving from descriptive statistics to effective risk modification.<\/jats:p>","DOI":"10.1111\/joim.70127","type":"journal-article","created":{"date-parts":[[2026,8,21]],"date-time":"2026-08-21T07:35:52Z","timestamp":1787297752000},"page":"553-571","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Sudden cardiac death in chronic kidney disease and dialysis: From descriptive epidemiology to mechanism\u2010driven prevention"],"prefix":"10.1111","volume":"300","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6616-1996","authenticated-orcid":false,"given":"Carmine","family":"Zoccali","sequence":"first","affiliation":[{"name":"Renal Research Institute  New York New York 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