Plasma hepcidin levels are elevated but responsive to erythropoietin therapy in renal disease

Hepcidin is a critical inhibitor of iron export from macrophages, enterocytes, and hepatocytes. Given that it is filtered and degraded by the kidney, its elevated levels in renal failure have been suggested to play a role in the disordered iron metabolism of uremia, including erythropoietin resistan...

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Published inKidney international Vol. 75; no. 9; pp. 976 - 981
Main Authors Ashby, Damien R., Gale, Daniel P., Busbridge, Mark, Murphy, Kevin G., Duncan, Neill D., Cairns, Tom D., Taube, David H., Bloom, Stephen R., Tam, Frederick W.K., Chapman, Richard S., Maxwell, Patrick H., Choi, Peter
Format Journal Article
LanguageEnglish
Published Basingstoke Elsevier Inc 01.05.2009
Nature Publishing Group
Elsevier Limited
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Abstract Hepcidin is a critical inhibitor of iron export from macrophages, enterocytes, and hepatocytes. Given that it is filtered and degraded by the kidney, its elevated levels in renal failure have been suggested to play a role in the disordered iron metabolism of uremia, including erythropoietin resistance. Here, we used a novel radioimmunoassay for hepcidin-25, the active form of the hormone, to measure its levels in renal disease. There was a significant diurnal variation of hepcidin and a strong correlation to ferritin levels in normal volunteers. In 44 patients with mild to moderate kidney disease, hepcidin levels were significantly elevated, positively correlated with ferritin but inversely correlated with the estimated glomerular filtration rate. In 94 stable hemodialysis patients, hepcidin levels were also significantly elevated, but this did not correlate with interleukin-6 levels, suggesting that increased hepcidin was not due to a general inflammatory state. Elevated hepcidin was associated with anemia, but, intriguingly, the erythropoietin dose was negatively correlated with hepcidin, suggesting that erythropoietin suppresses hepcidin levels. This was confirmed in 7 patients when hepcidin levels significantly decreased after initiation of erythropoietin treatment. Our results show that hepcidin is elevated in renal disease and suggest that higher hepcidin levels do not predict increased erythropoietin requirements.
AbstractList Hepcidin is a critical inhibitor of iron export from macrophages, enterocytes, and hepatocytes. Given that it is filtered and degraded by the kidney, its elevated levels in renal failure have been suggested to play a role in the disordered iron metabolism of uremia, including erythropoietin resistance. Here, we used a novel radioimmunoassay for hepcidin-25, the active form of the hormone, to measure its levels in renal disease. There was a significant diurnal variation of hepcidin and a strong correlation to ferritin levels in normal volunteers. In 44 patients with mild to moderate kidney disease, hepcidin levels were significantly elevated, positively correlated with ferritin but inversely correlated with the estimated glomerular filtration rate. In 94 stable hemodialysis patients, hepcidin levels were also significantly elevated, but this did not correlate with interleukin-6 levels, suggesting that increased hepcidin was not due to a general inflammatory state. Elevated hepcidin was associated with anemia, but, intriguingly, the erythropoietin dose was negatively correlated with hepcidin, suggesting that erythropoietin suppresses hepcidin levels. This was confirmed in 7 patients when hepcidin levels significantly decreased after initiation of erythropoietin treatment. Our results show that hepcidin is elevated in renal disease and suggest that higher hepcidin levels do not predict increased erythropoietin requirements.
Author Gale, Daniel P.
Taube, David H.
Tam, Frederick W.K.
Busbridge, Mark
Murphy, Kevin G.
Choi, Peter
Maxwell, Patrick H.
Chapman, Richard S.
Bloom, Stephen R.
Cairns, Tom D.
Ashby, Damien R.
Duncan, Neill D.
Author_xml – sequence: 1
  givenname: Damien R.
  surname: Ashby
  fullname: Ashby, Damien R.
  email: d.ashby@imperial.ac.uk
  organization: Imperial College Kidney and Transplant Institute, Hammersmith Hospital, Imperial College London, London, UK
– sequence: 2
  givenname: Daniel P.
  surname: Gale
  fullname: Gale, Daniel P.
  organization: Imperial College Kidney and Transplant Institute, Hammersmith Hospital, Imperial College London, London, UK
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  givenname: Mark
  surname: Busbridge
  fullname: Busbridge, Mark
  organization: Department of Clinical Chemistry, Hammersmith Hospital, Imperial College London, London, UK
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  givenname: Kevin G.
  surname: Murphy
  fullname: Murphy, Kevin G.
  organization: Department of Investigative Medicine, Hammersmith Hospital, Imperial College London, London, UK
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  givenname: Neill D.
  surname: Duncan
  fullname: Duncan, Neill D.
  organization: Imperial College Kidney and Transplant Institute, Hammersmith Hospital, Imperial College London, London, UK
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  givenname: Tom D.
  surname: Cairns
  fullname: Cairns, Tom D.
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  surname: Taube
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  surname: Bloom
  fullname: Bloom, Stephen R.
  organization: Department of Investigative Medicine, Hammersmith Hospital, Imperial College London, London, UK
– sequence: 9
  givenname: Frederick W.K.
  surname: Tam
  fullname: Tam, Frederick W.K.
  organization: Imperial College Kidney and Transplant Institute, Hammersmith Hospital, Imperial College London, London, UK
– sequence: 10
  givenname: Richard S.
  surname: Chapman
  fullname: Chapman, Richard S.
  organization: Department of Clinical Chemistry, Hammersmith Hospital, Imperial College London, London, UK
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  surname: Maxwell
  fullname: Maxwell, Patrick H.
  organization: Division of Medicine, University College London, London, UK
– sequence: 12
  givenname: Peter
  surname: Choi
  fullname: Choi, Peter
  organization: Imperial College Kidney and Transplant Institute, Hammersmith Hospital, Imperial College London, London, UK
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ISSN 0085-2538
IngestDate Wed Dec 04 07:22:45 EST 2024
Wed Nov 06 09:04:49 EST 2024
Fri Dec 06 01:48:53 EST 2024
Sat Sep 28 07:53:29 EDT 2024
Sun Oct 22 16:04:41 EDT 2023
Thu Oct 07 19:34:38 EDT 2021
Fri Feb 23 02:18:32 EST 2024
IsDoiOpenAccess true
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IsScholarly true
Issue 9
Keywords dialysis
iron
kidney disease
ferritin
hepcidin
erythropoietin
Kidney disease
Nephrology
Urinary system disease
Erythropoietin
Ferritin
Iron
Urology
Blood plasma
Nephropathy
Treatment
Polypeptide
Renal failure
Dialysis
Hepcidin
Language English
License http://www.elsevier.com/open-access/userlicense/1.0
CC BY 4.0
https://www.elsevier.com/tdm/userlicense/1.0
https://www.elsevier.com/open-access/userlicense/1.0
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Notes ObjectType-Article-2
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content type line 23
OpenAccessLink https://www.sciencedirect.com/science/article/pii/S0085253815538179
PMID 19212416
PQID 210124486
PQPubID 47198
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PublicationTitle Kidney international
PublicationTitleAlternate Kidney Int
PublicationYear 2009
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Snippet Hepcidin is a critical inhibitor of iron export from macrophages, enterocytes, and hepatocytes. Given that it is filtered and degraded by the kidney, its...
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SubjectTerms Adult
Aged
Aged, 80 and over
Anemia - metabolism
Antimicrobial Cationic Peptides - blood
Antimicrobial Cationic Peptides - drug effects
Biological and medical sciences
Case-Control Studies
Circadian Rhythm
dialysis
erythropoietin
Erythropoietin - pharmacology
Erythropoietin - therapeutic use
Female
ferritin
Ferritins - blood
Glomerular Filtration Rate
hepcidin
Hepcidins
Humans
iron
kidney disease
Kidney Diseases - blood
Kidney Diseases - drug therapy
Kidney Diseases - metabolism
Male
Medical sciences
Middle Aged
Nephrology. Urinary tract diseases
Nephropathies. Renovascular diseases. Renal failure
Radioimmunoassay
Recombinant Proteins
Renal failure
Young Adult
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Title Plasma hepcidin levels are elevated but responsive to erythropoietin therapy in renal disease
URI https://dx.doi.org/10.1038/ki.2009.21
http://dx.doi.org/10.1038/ki.2009.21
https://www.ncbi.nlm.nih.gov/pubmed/19212416
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