Hemodynamic and nonhemodynamic factors are implicated in the maintenance and aggravation of left ventricular (LV) hypertrophy in ESRD. Functional consequences of LV geometry are of substantial importance in patients who undergo dialysis and may contribute to explain the negative outcome related to LV hypertrophy, also in patients without overt coronary heart disease (CHD). Whereas most patients with eccentric LV hypertrophy have systolic dysfunction and the underlying CHD imposes progression of their disease, when overt CHD does not occur to remodel left ventricle, concentric LV geometry is more prevalent in ESRD and functional consequences are different. Concentric LV geometry is very sensitive to abrupt changes of cardiac loading conditions because of increased LV stiffness. Dialysis-related decrease in LV filling pressure reduces Starling forces recruitment and causes a fall in stroke volume as a result of reduced preload. This fall cannot be compensated by increased contractility, as myocardial mechanics is impaired in concentric LV geometry and no functional reserve can be used. When adequate increase in heart rate is not achieved to compensate reduced stroke volume, cardiac output substantially decreases and hypotension occurs. Occurrence of hypotension in the context of concentric LV geometry might contribute to reduce repeatedly coronary blood flow supply in the stiff and thick myocardium and might accelerate myocardial structural deterioration seen in ESRD.