Iron In AKI And In CKD

[ironjustice]

Iron metabolism in the pathogenesis of iron-induced kidney injury
Nature Reviews Nephrology
A. M. F. Martines, R. Masereeuw, H. Tjalsma, J. G. Hoenderop, J. F. M.
Wetzels & D. W. Swinkels

Abstract
In the past 8 years, there has been renewed interest in the role of
iron in both acute kidney injury (AKI) and chronic kidney disease
(CKD).
In patients with kidney diseases, renal tubules are exposed to a high
concentration of iron owing to increased glomerular filtration of iron
and iron-containing proteins, including haemoglobin, transferrin and
neutrophil gelatinase-associated lipocalin (NGAL).
Levels of intracellular catalytic iron may increase when glomerular
and renal tubular cells are injured.
Reducing the excessive luminal or intracellular levels of iron in the
kidney could be a promising approach to treat AKI and CKD.
Understanding the role of iron in kidney injury and as a therapeutic
target requires insight into the mechanisms of iron metabolism in the
kidney, the role of endogenous proteins involved in iron chelation and
transport, including hepcidin, NGAL, the NGAL receptor and divalent
metal transporter 1, and iron-induced toxic effects.
This Review summarizes emerging knowledge, which suggests that complex
mechanisms of iron metabolism exist in the kidney, modulated directly
or indirectly by cellular iron content, inflammation, ischaemia and
oxidative stress.
The potential exists for prevention and treatment of iron-induced
kidney injury by customized iron removal or relocation, aided by
detailed insight into the underlying pathological mechanisms.

doi:10.1038/nrneph.2013.98

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http://www.nature.com/nrneph/journal/vaop/ncurrent/full/nrneph.2013.98.html


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