Jönsson Sofia, Agic Mediha Becirovic, Narfström Fredrik, Melville Jacqueline M, Hultström Michael
Unit for Integrative Physiology, Department of Medical Cellbiology, Uppsala University, Uppsala, Sweden; and.
Unit for Anaesthesiology and Intensive Care, Department of Surgical Sciences, Uppsala University, Uppsala, Sweden.
Am J Physiol Regul Integr Comp Physiol. 2014 Sep 1;307(5):R493-7. doi: 10.1152/ajpregu.00178.2014. Epub 2014 Jun 11.
Decompensation in heart failure occurs when the heart fails to balance venous return with cardiac output, leading to fluid congestion and contributing to mortality. Decompensated heart failure can cause acute kidney injury (AKI), which further increases mortality. Heart failure activates signaling systems that are deleterious to kidneys such as renal sympathetic nerve activity (RSNA), renin-angiotensin-aldosterone system, and vasopressin secretion. All three reduce renal blood flow (RBF) and increase tubular sodium reabsorption, which may increase renal oxygen consumption causing AKI through renal tissue hypoxia. Vasopressin contributes to venous congestion through aquaporin-mediated water retention. Additional water retention may be mediated through vasopressin-induced medullary urea transport and hyaluronan but needs further study. In addition, there are several systems that could protect the kidneys and reduce fluid retention such as natriuretic peptides, prostaglandins, and nitric oxide. However, the effect of natriuretic peptides and nitric oxide are blunted in decompensation, partly due to oxidative stress. This review considers how neurohormonal signaling in heart failure drives fluid retention by the kidneys and thus exacerbates decompensation. It further identifies areas where there is limited data, such as signaling systems 20-HETE, purines, endothelin, the role of renal water retention mechanisms for congestion, and renal hypoxia in AKI during heart failure.
当心脏无法使静脉回流与心输出量保持平衡时，就会发生心力衰竭失代偿，进而导致液体潴留并增加死亡率。失代偿性心力衰竭可导致急性肾损伤（AKI），这会进一步增加死亡率。心力衰竭会激活对肾脏有害的信号系统，如肾交感神经活动（RSNA）、肾素 - 血管紧张素 - 醛固酮系统和抗利尿激素分泌。这三者都会减少肾血流量（RBF）并增加肾小管对钠的重吸收，这可能会增加肾脏的氧消耗，通过肾组织缺氧导致急性肾损伤。抗利尿激素通过水通道蛋白介导的水潴留导致静脉充血。额外的水潴留可能通过抗利尿激素诱导的髓质尿素转运和透明质酸介导，但需要进一步研究。此外，还有几个系统可以保护肾脏并减少液体潴留，如利钠肽、前列腺素和一氧化氮。然而，在失代偿状态下，利钠肽和一氧化氮的作用会减弱，部分原因是氧化应激。本综述探讨了心力衰竭中的神经激素信号如何驱动肾脏液体潴留，从而加剧失代偿。它还进一步确定了数据有限的领域，如信号系统20 - 羟基二十碳四烯酸（20-HETE）、嘌呤、内皮素、肾脏水潴留机制在充血中的作用以及心力衰竭期间急性肾损伤中的肾缺氧。
