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SGLT-2 Inhibitors in Heart Failure: Implications for the Kidneys

  • Pathophysiology of Myocardial Failure (Inder Anand and Maria Patarroyo-Aponte, Section Editors)
  • Published:
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Abstract

Purpose of Review

This review aims to summarize the renal effects of sodium-glucose transporter-2 (SGLT-2) inhibitors and their potential implications in heart failure pathophysiology.

Recent Findings

In patients with diabetes and established atherosclerosis, the SGLT-2 inhibitor empagliflozin versus placebo significantly reduced the rate of heart failure admissions with 35%. Moreover, empagliflozin slowed kidney disease progression and reduced the need for renal replacement therapy.

Summary

SGLT-2 inhibitors inhibit proximal tubular sodium and chloride reabsorption, leading to increased nephron flux throughout the distal renal tubules, most notably at the level of the macula densa. Afferent arteriolar vasoconstriction is promoted through tubulo-glomerular feedback and reduces glomerular capillary hydrostatic pressure, relieving podocyte stress and explaining renal preservation. Further, plasma volume is contracted and natriuresis promoted without inducing neurohumoral activation. Finally, SGLT-2 inhibitors may improve endothelial function and energy metabolism efficiency. Together, these promising features place them as a potential novel treatment for heart failure.

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Correspondence to Frederik H. Verbrugge.

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Frederik H. Verbrugge, Pieter Martens, and Wilfried Mullens declare no conflicts of interest.

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This article does not contain any studies with human or animal subjects performed by any of the authors.

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This article is part of the Topical Collection on Pathophysiology of Myocardial Failure

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Verbrugge, F.H., Martens, P. & Mullens, W. SGLT-2 Inhibitors in Heart Failure: Implications for the Kidneys. Curr Heart Fail Rep 14, 331–337 (2017). https://doi.org/10.1007/s11897-017-0345-9

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