London Gerard M
Centre Hospitalier FH MANHES, Fleury-Mérogis, France.
Nephrol Dial Transplant. 2002;17 Suppl 1:29-36. doi: 10.1093/ndt/17.suppl_1.29.
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.
慢性肾脏病和终末期肾病（ESRD）患者中左心室（LV）改变，尤其是左心室肥厚（LVH）的患病率很高。心室扩大通常与正常的收缩功能以及升高的中风和心脏指数有关。在没有内在心脏病的情况下，LV扩大很可能归因于与贫血、动静脉分流的存在以及钠和水潴留相关的慢性容量/血流超负荷。在ESRD患者中，高血压也是LVH的主要原因，但LV结构改变和心肌纤维化也可能归因于非血流动力学因素，如血管紧张素II、甲状旁腺激素、内皮素、醛固酮、交感神经放电增加和血浆儿茶酚胺增加。为改善ESRD的临床结局，通过纠正导致血流和压力超负荷的因素（包括贫血）来预防LVH及其并发症至关重要。
