Left ventricular alterations and end-stage renal disease

Abstract

The prevalence of left ventricular (LV) changes, especially LV hypertrophy (LVH), is high among patients with chronic kidney disease and end-stage renal disease (ESRD). Ventricular enlargement usually is associated with normal systolic function and increased stroke and cardiac index. In the absence of intrinsic heart disease, LV enlargement is most probably attributable to chronic volume/flow overload associated with anaemia, the presence of arteriovenous shunts, and sodium and water retention. In ESRD patients, hypertension is also a leading cause of LVH, but structural LV changes and myocardial fibrosis may also be due to non-haemodynamic factors such as angiotensin II, parathyroid hormone, endothelin, aldosterone, increased sympathetic nerve discharge and increased plasma catecholamines. To improve the clinical outcomes in ESRD, it is essential to prevent LVH and its complications by correcting the factors that contribute to flow and pressure overload, including anaemia.