ArticleEuropean heart journal2021
Compensatory post-diuretic renal sodium reabsorption is not a dominant mechanism of diuretic resistance in acute heart failure.
Article in European heart journal, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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15 citing papers in PubMed, 30 citations in OpenAlex.
- Effects of heart failure pharmacotherapy on natriuresis and diuresis: A narrative review.Heart failure reviews · 2026Review
- The 'Chloride Theory' for Heart Failure Pathophysiology: An Updated Narrative Review 2025.Cardiology and therapy · 2026Review
- Device therapies in cardiorenal syndrome: an expert review.ESC heart failure · 2026Review
- A Mechanistic Framework Integrating Renal QSP-PK-PD and Machine Learning for Baseline-Informed Stratification of Diuretic Resistance.The AAPS journal · 2026Article
- Adipokine profile in acute heart failure: associations with natriuretic response and prognosis.ESC heart failure · 2026Observational
- Peritoneal Dialysis Versus Extracorporeal Ultrafiltration Modalities in the Management of Acute Cardiorenal Syndrome with Diuretic Resistance.Life (Basel, Switzerland) · 2026Article
- Decongestion in heart failure: medical and device therapies.Nature reviews. Cardiology · 2025Review
- Diuretic treatment using the RenalGuard® system in patients hospitalized due to acute decompensated heart failure and characterization of the profile of patients with good and poor response to treatment - preliminary study.Cardiology journal · 2025Article
- Counteracting the Mechanisms of Heart Failure is the Most Effective Way to Decongest Patients while Improving Outcomes.Cardiac failure review · 2025Review
- The utility of urine sodium-guided diuresis during acute decompensated heart failure.Heart failure reviews · 2024Review
- Effect of Post-Loop Diuretic Urinary Sodium Level on Length of Stay and Rehospitalization in Acutely Decompensated Heart Failure Patients.Cardiology research · 2024Article
- Randomized controlled trial of urinE chemiStry guided aCute heArt faiLure treATmEnt (ESCALATE): Rationale and design.American heart journal · 2023Article
- Spot Urinary Sodium Measurements: the Future Direction of the Treatment and Follow-up of Patients with Heart Failure.Current heart failure reports · 2023Review
- Multimodal Strategies for the Diagnosis and Management of Refractory Congestion. An Integrated Cardiorenal Approach.Frontiers in physiology · 2022Review
- Renal sodium avidity, the prevailing renal target in heart failure.European heart journal · 2021Article
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16 authors at 6 institutions in 3 countries.
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Abstract
aimsIn healthy volunteers, the kidney deploys compensatory post-diuretic sodium reabsorption (CPDSR) following loop diuretic-induced natriuresis, minimizing sodium excretion and producing a neutral sodium balance. CPDSR is extrapolated to non-euvolemic populations as a diuretic resistance mechanism; however, its importance in acute decompensated heart failure (ADHF) is unknown. METHODS AND
resultsPatients with ADHF in the Mechanisms of Diuretic Resistance cohort receiving intravenous loop diuretics (462 administrations in 285 patients) underwent supervised urine collections entailing an immediate pre-diuretic spot urine sample, then 6-h (diuretic-induced natriuresis period) and 18-h (post-diuretic period) urine collections. The average spot urine sodium concentration immediately prior to diuretic administration [median 15 h (13-17) after last diuretic] was 64 ± 33 mmol/L with only 4% of patients having low (<20 mmol/L) urine sodium consistent with CPDSR. Paradoxically, greater 6-h diuretic-induced natriuresis was associated with larger 18-h post-diuretic spontaneous natriuresis (r = 0.7, P < 0.001). Higher pre-diuretic urine sodium to creatinine ratio (r = 0.37, P < 0.001) was the strongest predictor of post-diuretic spontaneous natriuresis. In a subgroup of patients (n = 43) randomized to protocol-driven intensified diuretic therapies, the mean diuretic-induced natriuresis increased three-fold. In contrast to the substantial decrease in spontaneous natriuresis predicted by CPDSR, no change in post-diuretic spontaneous natriuresis was observed (P = 0.47).
conclusionOn a population level, CPDSR was not an important driver of diuretic resistance in hypervolemic ADHF. Contrary to CPDSR, a greater diuretic-induced natriuresis predicted a larger post-diuretic spontaneous natriuresis. Basal sodium avidity, rather than diuretic-induced CPDSR, appears to be the predominant determinate of both diuretic-induced and post-diuretic natriuresis in hypervolemic ADHF.
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