Cardiac dysfunction is a key factor in the high morbidity and mortality rates seen in hemodialysis (HD) patients. Much of the dysfunction is manifest as adverse changes in cardiac and vascular structure prior to commencing dialysis. This adverse vascular remodeling arises as a dysregulation between pro- and antiproliferative signaling pathways in response to hemodynamic and nonhemodynamic factors. The HD procedure itself further promotes cardiomyopathy by inducing hypotension and episodic regional cardiac ischemia that precedes global dysfunction, fibrosis, worsening symptoms, and increased mortality. Drug-based therapies have been largely ineffective in reversing HD-associated cardiomyopathy, in part due to targeting single pathways of low yield. Few studies have sought to establish natural history and there is no framework of priorities for future clinical trials. Targeting intradialytic cardiac dysfunction by altering dialysate temperature, composition, or ultrafiltration rate might prevent the development of global cardiomyopathy, heart failure, and mortality through multiple pathways. Novel imaging techniques show promise in characterizing the physiological response to HD that is a unique model of repetitive ischemia-reperfusion injury. Reducing HD-associated cardiomyopathy may need a paradigm shift from empirical delivery of solute clearance to a personalized therapy balancing solute and fluid removal with microvascular protection. This review describes the evidence for intradialytic cardiac dysfunction outlining cardioprotective strategies that extend to multiple organs with potential impacts on exercise tolerance, sleep, cognitive function, and quality of life.
© 2016 Wiley Periodicals, Inc.