Introduction

The metabolic, neurohumoral, and hemodynamic milieu of renal insufficiency appears to accelerate the atherosclerotic process, cause vascular calcification, heighten the rates of plaque rupture, and very importantly worsens myocardial systolic and diastolic function. Because of long-standing hypertension, activation of the renin-angiotensin aldosterone system, and anemia, left ventricular hypertrophy (LVH) is common in chronic kidney disease (CKD) and end-stage renal disease (ESRD). As a result of ischemic heart disease, LVH, and electrolyte shifts, there are higher rates of arrhythmias (atrial, ventricular, heart block) and sudden cardiac death with ESRD. These arrhythmias occur at higher rates during hemodialysis. Lastly, although mainly coincident to the above processes, there is commonly aortic valve sclerosis and mitral annular calcification in ESRD which predispose patients to endocarditis.