Open AccessEffect of furosemide on body composition and urinary proteins that mediate tubular sodium and sodium transport—A randomized controlled trial
Author(s) -
Mose Frank Holden,
OczachowskaKulik Anna Ewa,
Fenton Robert Andrew,
Bech Jesper Nørgaard
Publication year - 2021
Publication title -
physiological reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 39
ISSN - 2051-817X
DOI - 10.14814/phy2.14653
Subject(s) - furosemide , endocrinology , chemistry , sodium , medicine , diuretic , diuresis , extracellular fluid , urinary system , excretion , renal function , extracellular , biochemistry , organic chemistry
Background Furosemide inhibits the sodium potassium chloride cotransporter (NKCC2) in the thick ascending limb of the loop of Henle and increases urinary water and sodium excretion. This study investigates the effect of furosemide on body composition estimated with multifrequency bioimpedance spectroscopy (BIS) technique and urinary proteins from NKCC2. Methods This study is a randomized, placebo‐controlled, crossover study where healthy subjects received either placebo or 40 mg furosemide on two separate occasions, where body composition with BIS, renal function, proteins from tubular proteins that mediate sodium and water transport, and plasma concentrations of vasoactive hormones were measured before and after intervention. Results We observed an expected increased diuresis with a subsequent reduction in bodyweight of (−1.51 ± 0.36 kg, p < .001) and extracellular water (ECW; −1.14 ± 0.23 L, p < .001) after furosemide. We found a positive correlation between the decrease in ECW and a decrease in bodyweight and a negative correlation between the decrease in ECW and the increase in urinary output. Intracellular water (ICW) increased (0.47 ± 0.28 L, p < .001). Urinary excretion of NKCC2 increased after furosemide and the increase in NKCC2 correlated with an increase in urine output and a decrease in ECW. Conclusion We found BIS can detect acute changes in body water content but the method may be limited to estimation of ECW. BIS demonstrated that furosemide increases ICW which might be explained by an extracellular sodium loss. Finally, urinary proteins from NKCC2 increases after furosemide with a good correlation with diuresis end the decrease in ECW.