In patients with terminal renal failure, left ventricular hypertrophy (LVH) is extremely common. It is found in approximately 60 to 80% of patients starting renal replacement therapy. The main causes of LVH are increased preload from hypervolemia and increased afterload from increased peripheral resistance, giving rise to a mixture of eccentric and concentric hypertrophy, but other factors (high cardiac output from anemia and arteriovenous (A-V) fistula, altered compliance of central arteries, and activation of local systems such as renin and endothelin) also play a role. The clinical importance of LVH derives from the fact that LVH is a predictor of cardiac death in dialyzed patients independent of blood pressure. LVH is accompanied by microvascular disease and by marked interstitial fibrosis (more than seen in non-renal patients with similar degrees of hypertension). Recent findings suggest that LV remodeling starts early and is seen even in normotensive patients with glomerulonephritis when GFR is still normal. The strategies to reduce LVH include reduction of hypervolemia, (near) normalization of hemoglobin and lowering of blood pressure, particularly by administration of angiotensin converting enzyme inhibitors.