Department of Internal Medicine and Metabolic Diseases, Cardiology Section, University of Siena, Siena, Italy.
Heart Fail Rev. 2011 Nov;16(6):503-8. doi: 10.1007/s10741-011-9267-x.
Heart failure may lead to acute kidney injury and vice versa. Chronic kidney disease may affect the clinical outcome in terms of cardiovascular morbidity and mortality while chronic heart failure may cause CKD. All these disorders contribute to the composite definition of cardio-renal syndromes. Renal impairment in HF patients has been increasingly recognized as an independent risk factor for morbidity and mortality; however, the most important clinical trials in HF tend to exclude patients with significant renal dysfunction. The mechanisms whereby renal insufficiency worsens the outcome in HF are not known, and several pathways could contribute to the "vicious heart/kidney circle." Traditionally, renal impairment has been attributed to the renal hypoperfusion due to reduced cardiac output and decreased systemic pressure. The hypovolemia leads to sympathetic activity, increased renin-angiotensin-aldosterone pathways and arginine-vasopressin release. All these mechanisms cause fluid and sodium retention, peripheral vasoconstriction and an increased congestion as well as cardiac workload. Therapy addressed to improve renal dysfunction, reduce neurohormonal activation and ameliorate renal blood flow could lead to a reduction in mortality and hospitalization in patients with cardio-renal syndrome.
心力衰竭可能导致急性肾损伤，反之亦然。慢性肾脏病可能会影响心血管发病率和死亡率的临床结局，而慢性心力衰竭可能导致慢性肾脏病。所有这些疾病都促成了心肾综合征的综合定义。在心力衰竭患者中，肾功能损害已被越来越多地认为是发病率和死亡率的独立危险因素；然而，心力衰竭的最重要临床试验往往排除了肾功能显著受损的患者。肾功能不全如何使心力衰竭的预后恶化尚不清楚，多种途径可能导致“恶性循环”。传统上，由于心输出量减少和全身血压降低，肾功能不全归因于肾脏灌注不足。低血容量导致交感神经活动增加、肾素-血管紧张素-醛固酮途径和精氨酸加压素释放增加。所有这些机制导致液体和钠潴留、外周血管收缩和充血增加以及心脏工作量增加。旨在改善肾功能、减少神经激素激活和改善肾血流量的治疗可能会降低心肾综合征患者的死亡率和住院率。
