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Schork, A. ; Eberbach, M.-L. ; Artunc, F. ; Bohnert, B.N. ; Eisinger, F. ; Heister, D.J. ; Vosseler, A. ; Nadalin, S.* ; Birkenfeld, A.L. ; Heyne, N. ; Guthoff, M.

SGLT2 inhibitors correct fluid overload in adult kidney transplant recipients-A prospective observational study.

Transpl. Int. 37:12879 (2024)
Verlagsversion DOI PMC
Open Access Gold (Paid Option)
Creative Commons Lizenzvertrag
In this longitudinal observational study, we measured urinary glucose concentration, body composition and volume status (bioimpedance spectroscopy) and plasma renin and aldosterone concentrations in n = 22 kidney transplant recipients (KTRs) initiating on SGLT2I at baseline (BL), and after 1 week and 1, 3, and 6 months. Estimated glomerular filtration rate (eGFR) decreased by -2 mL/min/1.73 m2 (IQR -10-0) after 1 week and remained stable thereafter. Urinary glucose concentration was 10 (3-24) g/g creatinine after 1 week and correlated with eGFR (r2 = 0.273; p = 0.057). SGLT2I did not affect HbA1c, fasting blood glucose, body weight, fat or lean mass. SGLT2I decreased fluid overload dependent on baseline overhydration (OH, r2 = 0.54, p = 0.0003) without occurrence of dehydration. Plasma aldosterone increased at day 7, while plasma renin did not change significantly. In conclusion, SGLT2I corrected fluid overload in patients with elevated overhydration at baseline, while in euvolemic KTRs fluid status remained stable without reduction of body water below the reference range, thus promoting the safety of SGLT2I therapy in patients following kidney transplantation. Glucosuria, together with effects of SGLT2I on blood glucose control and body weight, is attenuated in KTRs dependent on eGFR.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
Schlagwörter Sglt2 Inhibitor ; Bioimpedance Spectroscopy ; Fluid Overload ; Glucosuria ; Kidney Transplantation
ISSN (print) / ISBN 0934-0874
e-ISSN 1432-2277
Zeitschrift Transplant international
Quellenangaben Band: 37, Heft: , Seiten: , Artikelnummer: 12879 Supplement: ,
Verlag Wiley
Verlagsort Oxford
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Diabetes Research and Metabolic Diseases (IDM)