Is albumin transfusion indicated in a patient with heart failure with reduced ejection fraction (HFrEF) and hypoalbuminemia?

Albumin Transfusion is NOT Indicated in HFrEF with Hypoalbuminemia

Albumin transfusion should not be routinely administered to patients with HFrEF and hypoalbuminemia (albumin 1.8 g/dL), as there is no evidence supporting mortality or morbidity benefit, and major heart failure guidelines do not recommend this intervention.

Why Albumin Transfusion is Not Recommended

Absence of Guideline Support

• Neither the 2022 AHA/ACC/HFSA guidelines 1 nor the 2016 ESC guidelines 1 recommend albumin transfusion for patients with HFrEF and hypoalbuminemia
• The most recent 2025 ESC HFA consensus statement on HFrEF management 1 makes no mention of albumin supplementation as a therapeutic intervention
• Guidelines focus exclusively on evidence-based therapies including ACE inhibitors, beta-blockers, mineralocorticoid receptor antagonists, SGLT2 inhibitors, and ARNIs 1

Lack of Clinical Benefit from Research Evidence

• A 2022 retrospective cohort study of 1,038 hospitalized AHF patients found that albumin administration (median dose 29.0 g) showed no significant association with the composite endpoint of intubation, emergency renal replacement therapy, or death (HR 1.05,95% CI 0.75-1.47) 2
• This study specifically evaluated patients with lower baseline albumin levels (median 31.7 g/L in the albumin group vs 37.3 g/L in controls) and found no mortality benefit 2

What Hypoalbuminemia Actually Represents in HFrEF

Prognostic Marker, Not Treatment Target

• Hypoalbuminemia (albumin ≤3.4-3.5 g/dL) is present in 25-54% of HF patients and serves as an independent predictor of mortality, not a reversible cause 3, 4, 5
• In acute decompensated HF, hypoalbuminemia predicts 1-year mortality with an adjusted HR of 2.05 (95% CI 1.10-3.81) 3
• In chronic systolic HF, hypoalbuminemia carries a 1-year mortality risk-adjusted HR of 2.2 (95% CI 1.4-3.3) 4
• A large real-world cohort demonstrated that the lowest albumin quartile had an adjusted HR for mortality of 5.74 (95% CI 4.08-8.07) compared to the highest quartile 5

Associated Pathophysiology

• Hypoalbuminemia in HF reflects multiple detrimental processes including inflammation (elevated CRP), renal dysfunction, malnutrition, volume overload, and disease severity 3, 4, 5
• It correlates with higher NYHA class, elevated BNP, anemia, hyponatremia, and lower cholesterol 3, 4
• The prevalence ranges from 5-70% across the ejection fraction spectrum, being more common in elderly patients 6

What You Should Do Instead

Focus on Guideline-Directed Medical Therapy (GDMT)

• Initiate or optimize the four pillars of HFrEF therapy: ACE inhibitor/ARB/ARNI, beta-blocker, mineralocorticoid receptor antagonist, and SGLT2 inhibitor 1
• These therapies reduce mortality and HF hospitalization regardless of albumin levels 1

Manage Congestion Appropriately

• Use diuretics to reduce signs and symptoms of congestion 1
• The ESC guidelines note that increases in creatinine during decongestion with appropriate diuresis and hemoconcentration are not always clinically relevant 1

Address Underlying Causes

• Investigate reversible causes of hypoalbuminemia: malnutrition, inflammation, liver disease, protein-losing enteropathy, nephrotic syndrome 6
• Optimize nutritional status through appropriate dietary consultation, though evidence for nutritional supplementation improving HF outcomes remains unclear 6
• Treat comorbidities that worsen prognosis: chronic kidney disease (eGFR monitoring), anemia, diabetes (metformin should be considered unless contraindicated) 1

Monitor as a Prognostic Indicator

• Serial albumin measurements provide prognostic information: a decrease in albumin on follow-up independently predicts increased mortality (HR 2.58,95% CI 2.12-3.14) 5
• Use albumin trends to identify patients requiring more intensive monitoring and GDMT optimization 5

Critical Pitfall to Avoid

Do not mistake hypoalbuminemia as a therapeutic target requiring albumin replacement. The low albumin is a marker of disease severity and systemic derangement, not a deficiency state that responds to exogenous supplementation in the HF context. Your patient with albumin 1.8 g/dL needs aggressive GDMT optimization and investigation of reversible causes, not albumin infusion 2, 6.