Iron deficiency and supplementation in heart failure and chronic kidney disease

Area of Science:

• Cardiology
• Nephrology
• Biochemistry

Background:

• Iron deficiency (ID) is prevalent in heart failure (HF), impacting cellular respiration and mitochondrial function.
• Current ID management in HF often borrows from chronic kidney disease (CKD) protocols, despite differing pathophysiology.
• Intravenous (IV) iron supplementation is increasingly advocated for HF patients.

Purpose of the Study:

• To differentiate the mechanisms and pathophysiology of ID in HF versus CKD.
• To critically evaluate the evidence for IV iron supplementation in HF.
• To explore the potential role of novel oral iron formulations in HF management.

Main Methods:

• Review of regulatory mechanisms of iron metabolism in HF and CKD.
• Analysis of systemic and cellular differences in ID between HF and CKD populations.
• Examination of major clinical trials investigating IV iron in HF.

Main Results:

• IV iron supplementation in HF patients demonstrated symptomatic benefits but no improvement in clinical outcomes.
• High-dose IV iron administration bypasses normal regulatory pathways, potentially causing oxidative stress and damage to myocardium and endothelium.
• Newer oral iron preparations appear to lack the toxicity concerns associated with IV iron.

Conclusions:

• Significant differences exist in ID pathophysiology and regulation between HF and CKD.
• While IV iron may alleviate HF symptoms, its safety and efficacy for hard outcomes remain questionable due to potential toxicity.
• Oral iron supplementation represents a potentially safer and viable alternative for managing iron deficiency in heart failure.