10 myths about frusemide

Excerpt

Frusemide is the most frequently used diuretic in critically ill patients [1]. It exerts its action by selectively blocking the Na⁺/K⁺/2Cl⁻ co-transporter in the luminal membrane of the thick ascending limb of the loop of Henle (Supplementary Fig. S1). To reach the site of action, it is first taken up by the proximal cells via organic anion transporters and then secreted into the luminal space from where it is transported to the distal tubule. Frusemide generates greater loss of water than sodium loss, resulting in the production of hypotonic urine. Diuretic resistance is not uncommon in patients receiving prolonged therapy with loop diuretics. Furthermore, concern has been raised that diuretic use may be associated with harmful effects, including acute kidney injury (AKI). This has led to uncertainty among clinicians about when and how to use frusemide safely and effectively in critically ill patients with and without AKI [1]. Here, we address ten common myths about frusemide and its application in critically ill patients (Fig. 1).

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