In CKD, both high and low hepcidin tracked with worse outcomes

Design

Prospective cohort analysis

Population

3,826 adults with CKD in the CRIC study

Primary outcome

Heart failure, kidney outcomes, new diabetes

Effect

Highest vs middle tertile: kidney HR 1.19 (1.09-1.30); atherosclerotic HR 1.34 (1.09-1.64)

An analysis of the Chronic Renal Insufficiency Cohort, published in Kidney International on 20 October 2026, measured plasma hepcidin in 3,826 people with CKD and followed them for heart failure, kidney failure or halving of eGFR, new diabetes, atherosclerotic events and death.

Higher hepcidin went with older age, diabetes, lower eGFR, more albuminuria, higher iron indices and more inflammation. It was not associated with heart failure or new diabetes. Against the middle third, the highest third was associated with kidney outcomes (HR 1.19, 95% CI 1.09 to 1.30) and atherosclerotic events (HR 1.34, 1.09 to 1.64), and the lowest third with higher all-cause and cardiovascular mortality, after adjusting for iron and inflammation.

The U-shaped pattern suggests hepcidin reflects several processes rather than one. It is not a test for routine use, but it adds to the case that iron handling in CKD matters beyond anaemia.

• Do not order hepcidin routinely in CKD; it is a research marker.
• Assess iron status with ferritin and transferrin saturation as usual.
• Interpret ferritin with care in inflamed patients, where it may not reflect iron stores.
• Treat iron deficiency in CKD according to current guidance.

Why it matters

It hints that iron regulation links to kidney and vascular outcomes, not only to anaemia.

Don't overread it

Observational associations — it does not show that changing hepcidin would change outcomes.

The statistics, in plain English

A hazard ratio of 1.19 is a modest increase in risk. Comparing extreme thirds with the middle can exaggerate patterns, and a U-shape often reflects different underlying illnesses at each end.

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