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Prohepcidin, Inflammation and Iron Homeostasis in Hemodialysis Patients With Chronic Hepatitis C

This study has been completed.
Information provided by:
Istanbul University Identifier:
First received: January 6, 2011
Last updated: NA
Last verified: November 2009
History: No changes posted
The aim of this study is to address questions regarding the link among hepcidin, hematological iron markers, inflammation and hepatitis C in HD patients. In attempt to address this issue, we planned to measure serum levels of hepcidin prohormone (pro-hepcidin), inflammatory and iron parameters.

Renal Failure Chronic Requiring Hemodialysis Hepatitis C

Study Type: Observational
Study Design: Observational Model: Case Control
Time Perspective: Cross-Sectional
Official Title: Comparison of Prohepcidin, Inflammation and Iron Homeostasis in Hemodialysis Patients With and Without Chronic Hepatitis C

Resource links provided by NLM:

Further study details as provided by Istanbul University:

Primary Outcome Measures:
  • Association of prohepcidin and inflammation [ Time Frame: 3 months ]

Enrollment: 80
Study Start Date: August 2008
Study Completion Date: March 2010
Primary Completion Date: March 2010 (Final data collection date for primary outcome measure)
HCV (+)
Hemodialysis patients with chronic hepatitis C
HCV (-)
Hemodialysis patients without chronic hepatitis C
Healthy volunteers

Detailed Description:
Hepatitis C virus (HCV) infection is the most common cause of chronic liver disease in the world and also common among chronic hemodialysis (HD) patients. Patients with chronic HCV often have increased liver iron, a condition associated with reduced sustained response to antiviral therapy, more rapid progression to cirrhosis, and development of hepatocellular carcinoma; however, little is known about the mechanism of iron accumulation in the liver. Recently identified hepcidin, a 25-amino acid peptide hormone exclusively synthesized in the liver, is thought to be a key regulator for iron homeostasis and is induced by infection and inflammation. Hepcidin expression is modulated by iron stores, so that it decreases in iron deficiency to facilitate iron absorption while it increases in iron repletion to prevent pathological overload. Interleukin (IL)-6 has been proposed as a major inducer of hepcidin, via direct transcriptional activation of hepatic hepcidin expression by binding to its receptor complex containing gp130 to activate janus kinase (JAK) and activator of transcription 3 (STAT 3).

Ages Eligible for Study:   18 Years to 85 Years   (Adult, Senior)
Sexes Eligible for Study:   All
Accepts Healthy Volunteers:   Yes
Sampling Method:   Non-Probability Sample
Study Population
Patients on chronic hemodialysis

Inclusion Criteria:

  • Chronic hemodialysis patients

Exclusion Criteria:

  • Patients positive for hepatitis B virus surface antigen (HBsAg)
  • Patients previously diagnosed nonrenal cause of anemia other than iron deficiency
  • Patients with an evidence of active or occult bleeding
  • Patients received blood transfusion within the past 4 months
  • Patients with a history of malignancy, end-stage liver disease, or chronic hypoxia
  • Patients with a history of recent hospitalization or infection requiring antibiotics within the past 4 weeks.
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Please refer to this study by its identifier: NCT01272479

Division of Nephrology, Istanbul Faculty of Medicine
Istanbul, Turkey, 34390
Sponsors and Collaborators
Istanbul University
Principal Investigator: Yasar Caliskan MD
  More Information

Responsible Party: Istanbul University Scientific Research Projects, Istanbul University Identifier: NCT01272479     History of Changes
Other Study ID Numbers: 1692
Study First Received: January 6, 2011
Last Updated: January 6, 2011

Keywords provided by Istanbul University:
hepatitis C
iron stores

Additional relevant MeSH terms:
Hepatitis A
Hepatitis C
Hepatitis, Chronic
Hepatitis C, Chronic
Renal Insufficiency
Kidney Failure, Chronic
Liver Diseases
Digestive System Diseases
Hepatitis, Viral, Human
Virus Diseases
Enterovirus Infections
Picornaviridae Infections
RNA Virus Infections
Flaviviridae Infections
Pathologic Processes
Kidney Diseases
Urologic Diseases
Renal Insufficiency, Chronic
Anti-Infective Agents processed this record on July 24, 2017