The Benefit of Sodium-Glucose Co-Transporter Inhibition in Heart Failure: The Role of the Kidney

In the essential homeostatic role of kidney, two intrarenal mechanisms are prominent: the glomerulotubular balance driving the process of Na<sup>+</sup> and water reabsorption in the proximal tubule, and the tubuloglomerular feedback which senses the Na<sup>+</sup> concentrat...

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Main Authors: Edoardo Gronda, Emilio Vanoli, Massimo Iacoviello, Pasquale Caldarola, Domenico Gabrielli, Luigi Tavazzi
Format: Article
Language:English
Published: MDPI AG 2022-10-01
Series:International Journal of Molecular Sciences
Subjects:
Online Access:https://www.mdpi.com/1422-0067/23/19/11987
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author Edoardo Gronda
Emilio Vanoli
Massimo Iacoviello
Pasquale Caldarola
Domenico Gabrielli
Luigi Tavazzi
author_facet Edoardo Gronda
Emilio Vanoli
Massimo Iacoviello
Pasquale Caldarola
Domenico Gabrielli
Luigi Tavazzi
author_sort Edoardo Gronda
collection DOAJ
description In the essential homeostatic role of kidney, two intrarenal mechanisms are prominent: the glomerulotubular balance driving the process of Na<sup>+</sup> and water reabsorption in the proximal tubule, and the tubuloglomerular feedback which senses the Na<sup>+</sup> concentration in the filtrate by the juxtaglomerular apparatus to provide negative feedback on the glomerular filtration rate. In essence, the two mechanisms regulate renal oxygen consumption. The renal hyperfiltration driven by increased glomerular filtration pressure and by glucose diuresis can affect renal O<sub>2</sub> consumption that unleashes detrimental sympathetic activation. The sodium-glucose co-transporters inhibitors (SGLTi) can rebalance the reabsorption of Na<sup>+</sup> coupled with glucose and can restore renal O<sub>2</sub> demand, diminishing neuroendocrine activation. Large randomized controlled studies performed in diabetic subjects, in heart failure, and in populations with chronic kidney disease with and without diabetes, concordantly address effective action on heart failure exacerbations and renal adverse outcomes.
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spelling doaj.art-cd0c199e663647d4a0a53b31ac78962a2023-11-23T20:42:37ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672022-10-0123191198710.3390/ijms231911987The Benefit of Sodium-Glucose Co-Transporter Inhibition in Heart Failure: The Role of the KidneyEdoardo Gronda0Emilio Vanoli1Massimo Iacoviello2Pasquale Caldarola3Domenico Gabrielli4Luigi Tavazzi5Medicine and Medicine Sub-Specialties Department, Cardio Renal Program, UOC Nephrology, Dialysis and Adult Renal Transplant Program, IRCCS Ca’ Granda Foundation, Ospedale Maggiore Policlinico, 20122 Milano, ItalyU.O. Rehabilitative Cardiology Sacra Famiglia Hospital Fatebenefratelli, 22036 Erba, ItalyDepartment of Medical and Surgical Sciences, University of Foggia, 71122 Foggia, ItalyUOC Cardiology, Azienda Sanitaria Locale BA, 70132 Bari, ItalyUOC Cardiology, Azienda Ospedaliera San Camillo-Forlanini, 00152 Rome, ItalyMaria Cecilia Hospital, GVM Care & Research, 48033 Cotignola, ItalyIn the essential homeostatic role of kidney, two intrarenal mechanisms are prominent: the glomerulotubular balance driving the process of Na<sup>+</sup> and water reabsorption in the proximal tubule, and the tubuloglomerular feedback which senses the Na<sup>+</sup> concentration in the filtrate by the juxtaglomerular apparatus to provide negative feedback on the glomerular filtration rate. In essence, the two mechanisms regulate renal oxygen consumption. The renal hyperfiltration driven by increased glomerular filtration pressure and by glucose diuresis can affect renal O<sub>2</sub> consumption that unleashes detrimental sympathetic activation. The sodium-glucose co-transporters inhibitors (SGLTi) can rebalance the reabsorption of Na<sup>+</sup> coupled with glucose and can restore renal O<sub>2</sub> demand, diminishing neuroendocrine activation. Large randomized controlled studies performed in diabetic subjects, in heart failure, and in populations with chronic kidney disease with and without diabetes, concordantly address effective action on heart failure exacerbations and renal adverse outcomes.https://www.mdpi.com/1422-0067/23/19/11987sodium-glucose co-transporter-2inhibitorsSGLT2heart failurerenal failureglomerular filtration rate
spellingShingle Edoardo Gronda
Emilio Vanoli
Massimo Iacoviello
Pasquale Caldarola
Domenico Gabrielli
Luigi Tavazzi
The Benefit of Sodium-Glucose Co-Transporter Inhibition in Heart Failure: The Role of the Kidney
International Journal of Molecular Sciences
sodium-glucose co-transporter-2
inhibitors
SGLT2
heart failure
renal failure
glomerular filtration rate
title The Benefit of Sodium-Glucose Co-Transporter Inhibition in Heart Failure: The Role of the Kidney
title_full The Benefit of Sodium-Glucose Co-Transporter Inhibition in Heart Failure: The Role of the Kidney
title_fullStr The Benefit of Sodium-Glucose Co-Transporter Inhibition in Heart Failure: The Role of the Kidney
title_full_unstemmed The Benefit of Sodium-Glucose Co-Transporter Inhibition in Heart Failure: The Role of the Kidney
title_short The Benefit of Sodium-Glucose Co-Transporter Inhibition in Heart Failure: The Role of the Kidney
title_sort benefit of sodium glucose co transporter inhibition in heart failure the role of the kidney
topic sodium-glucose co-transporter-2
inhibitors
SGLT2
heart failure
renal failure
glomerular filtration rate
url https://www.mdpi.com/1422-0067/23/19/11987
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