Abstract

Furosemide, the most commonly used diuretic, has been proposed to improve renal medullary oxygenation. However, studies in patients with acute kidney injury (AKI) demonstrated that treatment with high doses of furosemide worsens renal function. In experimental sepsis, the rapid development of renal medullary hypoxia precedes the development of AKI and may contribute to its pathogenesis. We therefore investigated whether inhibiting active sodium transport and oxygen consumption in the medullary thick ascending limb with low-dose furosemide attenuates the medullary hypoxia in experimental septic AKI.

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