
Empagliflozin reduces markers of acute kidney injury in patients with acute decompensated heart failure
Author(s) -
Thiele Kirsten,
Rau Matthias,
Hartmann NielsUlrik Korbinian,
Möller Marcus,
Möllmann Julia,
Jankowski Joachim,
Keszei András P.,
Böhm Michael,
Floege Jürgen,
Marx Nikolaus,
Lehrke Michael
Publication year - 2022
Publication title -
esc heart failure
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.787
H-Index - 25
ISSN - 2055-5822
DOI - 10.1002/ehf2.13955
Subject(s) - empagliflozin , medicine , placebo , renal function , clinical endpoint , cardiology , acute kidney injury , diuresis , heart failure , hemodynamics , urology , randomized controlled trial , diabetes mellitus , type 2 diabetes , endocrinology , alternative medicine , pathology
Aims In this prospective, placebo‐controlled, double‐blind, exploratory study, we examined early and more delayed effects of empagliflozin treatment on haemodynamic parameters (primary endpoint: cardiac output) and kidney function including parameters of acute kidney injury (AKI) in patients with acute decompensated heart failure (HF). Methods and results Patients with acute decompensated HF with or without diabetes were randomized to empagliflozin 10 mg or placebo for 30 days. Haemodynamic, laboratory, and urinary parameters were assessed after 6 h, 1 day, 3 days, 7 days, and 30 days of treatment. Median time between hospital admission and randomization was 72 h. Baseline characteristics were not different in the empagliflozin ( n = 10) and placebo ( n = 9) groups. Empagliflozin led to a significant increase in urinary glucose excretion throughout the study (baseline: 37 ± 15 mg/24 h; Day 1: 14 565 ± 8663 mg/24 h; P = 0.001). Empagliflozin did not affect the primary endpoint of cardiac index or on systemic vascular resistance index at any time point. However, empagliflozin significantly reduced parameters of AKI (urinary TIMP‐2 and IGFBP7 by NephroCheck® as indicators of tubular kidney damage), which became significant after 3 days of treatment [placebo: 1.1 ± 1.1 (ng/mL) 2 /1000; empagliflozin: 0.3 ± 0.2 (ng/mL) 2 /1000; P = 0.02] and remained significant at the 7 day time point [placebo: 2.5 ± 3.8 (ng/mL) 2 /1000; empagliflozin: 0.3 ± 0.2 (ng/mL) 2 /1000; P = 0.003]. Conclusions In this study, empagliflozin treatment did not affect haemodynamic parameters but significantly reduced markers of tubular injury in patients with acute decompensated HF.