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|Title:||Does furosemide increase oxidative stress in acute kidney injury?|
|ANZCA/FPM Author:||Ho, KM|
|Keywords:||Acute Kidney Injury|
Acute Kidney Injury
|Citation:||Silbert BI, Ho KM, Lipman J, Roberts JA, Corcoran TB, Morgan DJ, Pavey W, Mas E, Barden AE, Mori TA. Does furosemide increase oxidative stress in acute kidney injury? Antioxid Redox Signal 2017;26(5):221-226.|
|Abstract:||Furosemide, a loop diuretic, is used to increase urine output in patients with acute kidney injury (AKI). It remains uncertain whether the benefits of furosemide in AKI outweigh its potential harms. We investigated if furosemide influenced oxidative stress in 30 critically ill patients with AKI by measuring changes in F2-isoprostanes (F2-IsoPs), markers of in vivo oxidative stress, in plasma and urine following intravenous furosemide. Urine F2-IsoPs were higher in sepsis (p = 0.001) and increased in proportion to urine furosemide (p = 0.001). The furosemide-induced increase in urine F2-IsoPs differed depending on AKI severity (p < 0.001) and was greatest in those with the most severe AKI. Furosemide had no effect on plasma F2-IsoPs. We demonstrate for the first time that furosemide increases renal oxidative stress in AKI and find that patients with the most severe AKI-to whom the largest doses are likely to be administered-showed the greatest increase in oxidative stress. These findings lead to the hypothesis that the common practice of administering high-dose furosemide to convert oliguric to nonoliguric AKI may induce harmful oxidative stress in the kidneys, and an adequately powered, randomized controlled trial is required to determine if clinical benefits of this dosing strategy justify its potential harms.|
|Journal Title:||Antioxidants & redox signaling|
|Affiliates:||Australian and New Zealand College of Anaesthetists|
|Appears in Collections:||Scholarly and Clinical|
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