What question did this study set out to answer?

To determine the role of distal tubular sodium reabsorption in diuretic resistance during heart failure treatment.

July 24, 2017Journal of the American Society of NephrologyOpen Access

Compensatory Distal Reabsorption Drives Diuretic Resistance in Human Heart Failure

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Why the study?

Does compensatory distal tubular sodium reabsorption drive diuretic resistance in human heart failure patients receiving loop diuretics?

Key Points

To determine the role of distal tubular sodium reabsorption in diuretic resistance during heart failure treatment.
Analyzed 128 heart failure patients treated with loop diuretics at Yale Transitional Care Center.
Measured fractional excretion of lithium (FELi) and fractional excretion of sodium (FENa) to evaluate sodium handling after diuretic administration.
Compared FELi and FENa in heart failure patients with a control group not receiving diuretics (n=52).
Mean prediuretic FELi was 16.2% in heart failure patients compared to 16.6% in control, P=0.82.
Diuretic administration increased FELi by 12.6% (P<0.001) while FENa increased only by 4.8% (SD 3.3%).
Only 34% of expected sodium release from diuretics reached urine due to distal tubular reabsorption, explaining only 6.4% of FENa increase (P=0.002).

Structured PICO

Does compensatory distal tubular sodium reabsorption drive diuretic resistance in human heart failure patients receiving loop diuretics?

Population

128 consecutive patients with heart failure receiving treatment with loop diuretics at the Yale Transitional Care Center, and a control cohort of 52 patients without heart failure not receiving diuretics.

Intervention

Intravenous furosemide equivalents (median 160 mg, interquartile range 40-270 mg).

Comparator

Pre-diuretic baseline state and a control cohort without heart failure not receiving diuretics.

Outcome

Fractional excretion of lithium (FELi) to assess proximal tubular and loop of Henle sodium handling, and fractional excretion of sodium (FENa) to assess net sodium excreted into the urine.surrogate

In human heart failure, diuretic resistance is primarily driven by compensatory distal tubular sodium reabsorption rather than a failure of loop diuretics to block sodium uptake in the loop of Henle.

Discussion

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Implication

Distal reabsorption may limit loop diuretic natriuresis in HF; leaves open whether distal blockade improves outcomes.

Cite This Study

Rao et al. (2017) studied this question.

synapsesocial.com/papers/69c8dd00ff3335695aa2e1b6 https://doi.org/10.1681/asn.2016111178

Topics

HFrEF treatment Heart failure

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Compensatory Distal Reabsorption Drives Diuretic Resistance in Human Heart Failure

Key Points

Structured PICO

Discussion

Implication

Cite This Study

Topics

Compensatory Distal Reabsorption Drives Diuretic Resistance in Human Heart Failure

Key Points

Structured PICO

Discussion

Implication

Cite This Study

Also Consider

Topics

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