Patients with end-stage renal disease (ESRD) experience a variety of hemodynamic and metabolic abnormalities that predispose to alterations in cardiac performance and morphology. High cardiac output related to renal anemia, hypertension, volume overload, and the arteriovenous fistula (in patients on hemodialysis) predispose to eccentric left ventricular (LV) hypertrophy. Hypertension, aortic stiffness, and aortic stenosis predispose to concentric LV hypertrophy. Most ESRD patients have a hybrid form of LV hypertrophy. LV hypertrophy is commonly accompanied by LV diastolic dysfunction. LV systolic dysfunction is less common. Newer dialytic techniques, excellent control of hypertension, and correction of renal anemia produce regression of LV hypertrophy. The effect of these interventions on LV systolic and diastolic function is less well established. Alterations in serum calcium, choice of dialysate base, hypoxia, and comorbid conditions may influence the effects of dialysis (particularly hemodialysis) on LV function. A variety of negative inotropic drugs may depress LV function in patients with ESRD.