Hepcidin—A Potential Novel Biomarker for Iron Status in Chronic Kidney Disease

Zaritsky, Joshua J.; Young, Brian; Wang, He Jing; Westerman, Mark; Olbina, Gordana; Nemeth, Elizabeta; Ganz, Tomas; Rivera, Seth; Nissenson, Allen R.; Salusky, Isidro B.

doi:10.2215/cjn.05931108

Cited by 296 publications

(310 citation statements)

References 35 publications

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“…Nevertheless, the majority of studies available until the beginning of this year have reported increased pre-dialytic serum hepcidin levels in CHD patients as compared to controls [10 -12, 14 -20]. It has therefore been hypothesized that in CHD patients increased hepcidin could aggravate functional iron deficiency by decreasing macrophage iron release and intestinal iron absorption, paving the way to the possible utilization of anti-hepcidin drugs for optimizing the management of anemia [9,21]. In regards to this point, it is of interest to note that administration of erythropoiesis stimulating agents (ESAs), by itself, has been reported to reduce hepcidin in patients with chronic kidney disease [15,22].…”

Section: Hepcidin As a Player In The Anemia Of Chdmentioning

confidence: 99%

Hepcidin levels in chronic hemodialysis patients: a critical evaluation

Valenti

Pelusi

Campostrini

et al. 2014

Clinical Chemistry and Laboratory Medicine

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Altered systemic iron metabolism is a key element of uremia, and functional iron deficiency mainly related to subclinical inflammation makes it difficult to maintain proper control of anemia in chronic hemodialysis patients (CHD). In the last decade, the hepatic hormone hepcidin has been progressively recognized as the master regulator of circulating iron levels through the modulation of cellular iron fluxes in response to iron stores, as well as to erythroid and inflammatory stimuli. Hepcidin is cleared by the kidney and progression of renal disease has been associated to increased serum hepcidin levels. This, in turn, reduces iron availability for erythropoiesis, suggesting anti-hepcidin strategies for improving anemia control. Moreover, hepcidin has been recently implicated in the pathogenesis of long-term complications of dialysis, like accelerated atherosclerosis. Initial studies almost invariably reported a sustained increase of serum hepcidin in chronic hemodialysis patients. Noteworthy, such studies included relatively few patients and controls that were poorly matched for major determinants of serum hepcidin at population level, i.e., age and gender. More recent data based on accurately matched larger series challenge the view that hepcidin is intrinsically increased in hemodialysis patients, showing a marked inter-and intra-individual variability of hormone levels. Here we take a critical look to the data published so far on hepcidin levels in CHD, analyze the reasons underlying the discrepancies in available studies and the hepcidin variability in CHD, and point out the need for further studies in large series of well-characterized CHD patients and controls.

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Section: Hepcidin As a Player In The Anemia Of Chdmentioning

confidence: 99%

Hepcidin levels in chronic hemodialysis patients: a critical evaluation

Valenti

Pelusi

Campostrini

et al. 2014

Clinical Chemistry and Laboratory Medicine

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“…Chronic kidney disease A role for hepcidin as a biomarker of chronic kidney disease (CKD) has also been proposed [16]. The increase in hepcidin concentrations with diminishing renal function in patients with CKD is believed to be the underlying mechanism behind ineffective erythropoiesis and erythropoietin (EPO) resistance [17].…”

Section: American Journal Of Hematologymentioning

confidence: 99%

Peering into the future: Hepcidin testing

2013

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Hepcidin, a small 25 amino acid peptide, has been well established as the iron regulatory hormone. Its expression is upregulated in response to iron and inflammatory cytokines, and downregulated in anemic or hypoxic states. Hepcidin decreases iron export into the plasma by binding to and inducing the degradation of ferroportin, an iron channel located on macrophages and the basolateral surface of enterocytes. This leads to decreased absorption of parental iron by the enterocytes, reduced recycling of erythrocyte iron by macrophages, and increased iron stores in the hepatocytes. Although hepcidin assays are not currently approved for clinical use in the United States, there is much interest in the potential use of this biomarker for management of iron related medical conditions. This review briefly summarizes the current hepcidin test platforms under investigation and the challenges associated with development of a clinical assay for this biomarker. In addition, selected potential future applications hepcidin testing in the clinical setting are addressed. Am. J.

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“…In CKD patients, hepcidin levels ranged from 3 to 153 ng/ml with a median of 26.5 ng/ml, and in hemodialysis patients, hepcidin levels ranged from 25 to 159 ng/ml with a median of 59 ng/ml. Zaritsky et al (12) reported a median hepcidin value of 270 ng/ml in adult CKD patients and a value of 73 ng/ml in healthy volunteers.…”

Section: Elisamentioning

confidence: 99%

Current Status of the Measurement of Blood Hepcidin Levels in Chronic Kidney Disease

Macdougall¹,

Małyszko²,

Hider³

et al. 2010

Clinical Journal of the American Society of Nephrology

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Hepcidin is a small defensin-like peptide produced in the liver in response to anemia, hypoxia, or inflammation. In addition to its anti-microbial properties, it has also been found to be a key regulator of iron utilization, providing increased understanding of why chronic kidney disease patients absorb iron poorly from the gut and also why many hemodialysis patients develop functional iron deficiency in the presence of inflammation. Hepcidin synthesis is upregulated in uremia, as in other inflammatory states. The ability to measure hepcidin in biologic fluids has stimulated interest in the potential applicability of this measurement as a more informative marker of iron status than the traditional iron indices such as serum ferritin and transferrin saturation. Until recently, however, the assays for measuring hepcidin have lacked precision, accuracy, and internal validation. Over the last few years, however, several assays have become available that address these limitations. Broadly speaking, these can be divided into radioimmunoassays, ELISAs, and mass spectrometry methods. The purpose of this review is to outline the various assays available at the present time, to critique their advantages and limitations, and to report comparative data in patients with chronic kidney disease. A concern with the immunoassays is that they detect more than biologically active hepcidin-25. Mass spectrometric assays are specific for hepcidin-25 but are labor intensive and require more costly and sophisticated instrumentation. Thus, although mass spectrometry is more accurate, it is less practical for routine clinical use at the present time.

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Hepcidin—A Potential Novel Biomarker for Iron Status in Chronic Kidney Disease

Cited by 296 publications

References 35 publications

Hepcidin levels in chronic hemodialysis patients: a critical evaluation

Hepcidin levels in chronic hemodialysis patients: a critical evaluation

Peering into the future: Hepcidin testing

Current Status of the Measurement of Blood Hepcidin Levels in Chronic Kidney Disease

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