Heart Failure Reviews · Oct 24, 2026

Diuretic therapy at the heart-kidney interface: from acute decongestion to long-term de-escalation in heart failure with reduced ejection fraction

By Tsalouchos A, Dattolo PC

Loop diuretics remain the cornerstone of decongestion in acute heart failure, yet their use in heart failure with reduced ejection fraction (HFrEF) is obscured by two competing errors: undertreating congestion because serum creatinine rises, and continuing or escalating diuretics after euvolaemia. This narrative review integrates established evidence and contemporary guidance into a phase-based cardiorenal decision framework. Congestion is framed as a continuum generated by sodium retention, redistribution of stressed blood volume, vascular and ventricular compliance, right-sided pressure, and renal sodium avidity-not as a binary distinction between pressure and volume overload. During acute decompensation, intravenous loop diuretics remain first-line therapy; early urine output and spot urinary sodium can identify inadequate response and support protocolized escalation. Acetazolamide or a thiazide-type diuretic can improve decongestion when loop response is insufficient, although renal and electrolyte surveillance is essential. Sodium-glucose cotransporter 2 inhibitors should be initiated for disease modification after stabilization, but their context-dependent natriuretic effect does not replace loop diuretics in marked congestion. A creatinine rise during effective decongestion should be interpreted with residual congestion, haemodynamics, urine output, electrolytes, and evidence of kidney injury rather than through a universal threshold. After stabilization, implementation of foundational HFrEF therapy and reassessment of the minimum effective loop dose become priorities. Studies suggest that dose reduction or withdrawal is feasible in stable, euvolaemic patients, but event-powered evidence and validated outpatient biomarkers are lacking. Diuretics and disease-modifying therapy therefore have complementary, time-dependent roles: remove sodium when congestion is present, protect the kidney while recognizing hypoperfusion and intrinsic kidney injury, and de-escalate only after euvolaemia.

doi.org/10.1007/s10741-026-10689-1PubMed 42925351Interventions