——美国爱德华心脏医院Advocate心脏研究所Maria Rosa Costanzo教授专访

　　编者按：随着心血管疾病及肾脏病发生及发展机制的深入研究，人们越来越多聚焦心肾共患疾病，即心肾综合征。2016年4月2~4日，第65届美国心脏病学学会（ACC）2016科学年会上，有多个专题是关于心肾综合征的管理。对此，《国际循环》记者在会议现场也采访了美国爱德华心脏医院Advocate心脏研究所医学主任兼中西部心脏专家心力衰竭（心衰）项目主任Maria Rosa Costanzo教授。

　　心肾综合征的机制及分类进展

　　实际上，心肾综合征的定义非常广泛，它泛指心衰及除心衰之外其他情况下心脏与肾脏的相互作用。心肾综合征分类时最重要的是基于这两种器官何者首先启动了该病的发生。此外，还可根据发病急缓分类。具体来说，通常所说的1型心肾综合征指的是急性失代偿性心衰时心脏与肾脏的相互作用，其发生机制一方面是心衰失代偿导致神经内分泌激活加剧，进而引发肾脏血液动力学变化；另一方面，肾脏本身受交感神经支配，可产生肾素，心衰时心脏与肾脏的交互作用最终导致水钠潴留。2型心肾综合征指的是在慢性心衰患者中随时间推移所发生的肾功能变化，通常是由长期充血导致中心静脉压增加所致；中心静脉压增加可导致肾静脉高压，肾静脉高压可反过来导致肾间质静水压增加，当肾间质静水压超过肾小管压力时则可导致肾小管崩解。不论急性还是慢性心肾综合征，其治疗目标都是减少充血。

　　心肾综合征管理策略的特殊性

　　针对伴有心衰的心肾综合征患者，我们有必要开展更深入研究。对于这类患者的治疗，我常采用右心导管测量其心内压力以指导治疗。换句话说，我会在调整药物治疗前先了解患者的充血状态。就利尿剂而言，我更倾向选择生物利用度较高、作用持续时间较长者。因此，若合并心衰的心肾综合征患者既往应用呋塞米，我会换用托拉塞米，因为后者的生物利用度更好，作用时间更长。此外，这些患者常伴有利尿剂抵抗，大多是由于长期应用袢利尿剂导致钠盐无法在髓袢升支被重吸收而进入远端肾小管，从而导致远端肾小管本身需超负荷处理更多钠盐，引起肾小管肥大，进而影响袢利尿剂的作用。因此，这些患者需要序贯肾阻断治疗，选择噻嗪类利尿剂或盐皮质激素受体拮抗剂与袢利尿剂联用。我们推荐患者在应用袢利尿剂前30~60分钟应用噻嗪类利尿剂，从而阻断远端肾小管的适应机制，增加袢利尿剂疗效。

　　利尿剂在心肾综合征治疗中的地位

　　心衰专家对此尚未达成共识。对伴有心衰的心肾综合征患者，我会非常谨慎。尽管ACEI或ARB类药物会通过影响血液动力学而非直接毒性作用使患者肾功能轻度恶化，但我仍多次尝试使用这两种药物。有研究发现，ACEI、ARB及盐皮质激素受体拮抗剂具有肾脏保护作用，可减少蛋白尿。需特别注意的是，合并心衰的心肾综合征患者更易发生高钾血症，故需更密切监测并及时调整治疗药物。一旦发生高钾血症，要及时治疗。

原文：

　　Cardiorenal syndrome is actually a very broad definition， we indicate all the mutual interactions that occur between the heart and the kidney in the setting of heart failure and outside of the setting as well. The most important attempt at classification is based on which of the two organs initiates it， the heart or the kidney， based on whether in a setting which is acute or chronic. Cardiorenal syndrome type 1 is the mutual interactions between the heart and the kidney in the setting of acutely decompensated heart failure， the mechanisms in this case are when a patient with heart failure decompensate， there is a escalation of neural hormonal activation which causes profound hemodynamic chances in the kidney and vice versa. The kidney itself is a highly innervated organ with sympathetic nerves which produces rennin， the mutual interaction ultimately results in additional sodium and water retention. Cardiorenal syndrome type 2 is the renal function changes over time in patients with chronic heart failure. This is most often due to congestion with central venous pressure increase chronically， when translates into renal venous hypertension， it in turn causes an increase in the hydrostatic pressure of the renal interstitial， if this exceeds the pressure in the tubules， it could cause the tubules to collapse. Both in the acute and in the chronic setting， the goal of therapy is reducing congestion.

　　I think patients with heart failure and cardiorenal syndrome deserve to be studied in greater depth. I have a very low threshold to perform a right heart catheterization and measure intracardiac pressures to guide therapy. As far as diuretics， I prefer to use diuretics that have a high bioavailability and a longer duration of action. If they are on furosemide， I switch it to torsemide. Also these patients tend to have diuretic resistance which in most cases are caused by the chronic use of loop diuretics， because salt that not reabsorbed in the ascending loop of Henley reaches the distal tubules， the distal tubules have to handle a lot more sodium than they are used to， they undergo hypertrophy， so those patients require sequential nephronal blockage by using a thiazide diuretic or a mineral corticoid antagonist with the loop diuretic. We recommend they take the thiazide diuretic 30 to 60 minutes before the loop diuretic， this could block the adaptation mechanism in the distal tubules and increase the efficacy of the loop diuretic.