Abstract
Little is known about the mechanisms underlying loop diuretic resistance (DR) in heart failure (HF). Specifically, it is unclear if DR is primarily the result of resistance at the sight of tubular action in the loop of Henle, or whether it is mainly due to downstream compensatory sodium reabsorption in the distal tubule. Defining the mechanism of DR could guide therapy since treatment options differ substantially based on tubular location of resistance.
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