title: Renal neurohormonal regulation in heart failure decompensation.
abstract: 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.
authors.affiliation: Unit for Integrative Physiology, Department of Medical Cellbiology, Uppsala University, Uppsala, Sweden; and.
authors.forename: Sofia
authors.initials: S
authors.lastname: Jönsson
authors.affiliation: Unit for Integrative Physiology, Department of Medical Cellbiology, Uppsala University, Uppsala, Sweden; and.
authors.forename: Mediha Becirovic
authors.initials: MB
authors.lastname: Agic
authors.affiliation: Unit for Anaesthesiology and Intensive Care, Department of Surgical Sciences, Uppsala University, Uppsala, Sweden.
authors.forename: Fredrik
authors.initials: F
authors.lastname: Narfström
authors.affiliation: Unit for Integrative Physiology, Department of Medical Cellbiology, Uppsala University, Uppsala, Sweden; and.
authors.forename: Jacqueline M
authors.initials: JM
authors.lastname: Melville
authors.affiliation: 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 michael.hultstrom@mcb.uu.se.
authors.forename: Michael
authors.initials: M
authors.lastname: Hultström
mesh_terms: D058186:Acute Kidney Injury / Q000209:etiology / Q000503:physiopathology; D000818:Animals; D002302:Cardiac Output / Q000502:physiology; D006333:Heart Failure / Q000150:complications / Q000503:physiopathology*; D006801:Humans; D007668:Kidney / Q000294:innervation / Q000502:physiology*; D018377:Neurotransmitter Agents / Q000502:physiology*; D015398:Signal Transduction / Q000502:physiology; D013564:Sympathetic Nervous System / Q000502:physiology; D014882:Water-Electrolyte Balance / Q000502:physiology
chemical_list: D018377:Neurotransmitter Agents
keywords: ADHF; GFR; acute renal failure; cardiorenal syndrome; glomerular filtration rate