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A re-appraisal of volume status and renal function impairment in chronic heart failure: combined effects of pre-renal failure and venous congestion on renal function

机译:慢性心力衰竭患者的体积状态和肾功能损害的重新评估:肾功能衰竭和静脉充血对肾功能的综合影响

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摘要

The association between cardiac failure and renal function impairment has gained wide recognition over the last decade. Both structural damage in the form of systemic atherosclerosis and (patho) physiological hemodynamic changes may explain this association. As regards hemodynamic factors, renal impairment in chronic heart failure is traditionally assumed to be mainly due to a decrease in cardiac output and a subsequent decrease in renal perfusion. This will lead to a decrease in glomerular filtration rate and a compensatory increase in tubular sodium retention. The latter is a physiological renal response aimed at retaining fluids in order to increase cardiac filling pressure and thus renal perfusion. In heart failure, however, larger increases in cardiac filling pressure are needed to restore renal perfusion and thus more volume retention. In this concept, in chronic heart failure, an equilibrium exists where a certain degree of congestion is the price to be paid to maintain adequate renal perfusion and function. Recently, this hypothesis was challenged by new studies, wherein it was found that the association between right-sided cardiac filling pressures and renal function is bimodal, with worse renal function at the highest filling pressures, reflecting a severely congested state. Renal hemodynamic studies suggest that congestion negatively affects renal function in particular in patients in whom renal perfusion is also compromised. Thus, an interplay between cardiac forward failure and backward failure is involved in the renal function impairment in the congestive state, presumably along with other factors. Only few data are available on the impact of intervention in volume status on the cardio-renal interaction. Sparse data in cardiac patients as well as evidence from cohorts with primary renal disease suggest that specific targeting of volume overload may be beneficial for long-term outcome, in spite of a certain further decrease in renal function, at least in the context of current treatment where possible reflex neurohumoral activation is ameliorated by the background treatment by blockers of the renin–angiotensin–aldosterone system.
机译:在过去的十年中,心力衰竭与肾功能损害之间的关联得到了广泛的认可。系统性动脉粥样硬化形式的结构性损伤和(病理性)生理性血液动力学变化均可解释这种关联。关于血液动力学因素,传统上认为慢性心力衰竭的肾功能不全主要是由于心输出量减少以及随后的肾灌注减少所致。这将导致肾小球滤过率降低和肾小管钠sodium留的代偿性增加。后者是生理性肾脏反应,旨在保留体液,以增加心脏充盈压,从而增加肾脏灌注。然而,在心力衰竭中,需要更大的心脏充盈压增加来恢复肾脏灌注,从而保留更多的体积。在这个概念中,在慢性心力衰竭中,存在一种平衡,其中一定程度的充血是维持足够的肾脏灌注和功能所要付出的代价。最近,这一假设受到新研究的挑战,其中发现右侧心脏充盈压与肾功能之间的关系是双峰的,在最高充盈压下肾功能较差,反映出严重的充血状态。肾脏血液动力学研究表明,充血会对肾脏功能产生负面影响,特别是在肾脏灌注也受到损害的患者中。因此,在充血状态的肾功能损害中,可能与其他因素一起涉及心脏前向衰竭和向后衰竭之间的相互作用。关于干预量状态对心肾互动影响的数据很少。心脏病患者的稀疏数据以及原发性肾脏疾病队列的证据表明,尽管肾功能进一步下降,至少在目前治疗的背景下,针对容量超负荷的特异性靶向可能有益于长期预后通过阻断肾素-血管紧张素-醛固酮系统的背景治疗,可以改善反射神经体液的激活。

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