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Indoxyl Sulfate Induces Leukocyte-endothelial Interactions Through Up-regulation of ICAM-1 in Acute Kidney Injury

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ClinicalTrials.gov Identifier: NCT02061566
Recruitment Status : Unknown
Verified February 2014 by National Taiwan University Hospital.
Recruitment status was:  Not yet recruiting
First Posted : February 13, 2014
Last Update Posted : February 25, 2014
Sponsor:
Information provided by (Responsible Party):
National Taiwan University Hospital

Brief Summary:
Indoxyl sulfate (IS) is an anionic uremic toxin that is accumulated in the serum of patients with uremia. In previous study, the investigators successfully induced AKI animal model. IS enhanced intercellular adhesion molecule-1 (ICAM-1) expression in IL-1β-treated human umbilical vein endothelial cells (HUVECs) that this may play a critical role in the progression of AKI. However, the molecular mechanisms of ICAM-1 expression in IS-treated IL-1β-treated HUVECs need to be elucidated. HUVECs incubated with 0.2 or 1 mM IS for 24 h did not cause cytotoxicity. The IL-1β-induced ICAM-1 expression in HUVECs was significantly enhanced by IS pretreatment. Furthermore, the regulation of adhesion molecule expression involves a complex array of intracellular signaling pathways including mitogen-activated protein kinase (MAPKs), reactive oxygen species (ROS) and transcriptional factors. A better understanding of this might provide important insights into the prevention of AKI.

Condition or disease
Renal Function Disorder

Detailed Description:
Over the past decade, acute kidney injury (AKI) has acquired much attention because of their potentially devastating problems in clinical medicine. When kidneys lost their filtering function, a lot of dangerous metabolites were accumulated in the body, including urea, nitrogenous waste products and uremic toxins. Indoxyl sulfate (IS) is an anionic uremic toxin that is accumulated in the serum of patients with uremia. In previous study, the investigators successfully induced AKI animal model. IS enhanced intercellular adhesion molecule-1 (ICAM-1) expression in IL-1β-treated human umbilical vein endothelial cells (HUVECs) that this may play a critical role in the progression of AKI. However, the molecular mechanisms of ICAM-1 expression in IS-treated IL-1β-treated HUVECs need to be elucidated. HUVECs incubated with 0.2 or 1 mM IS for 24 h did not cause cytotoxicity. The IL-1β-induced ICAM-1 expression in HUVECs was significantly enhanced by IS pretreatment. Furthermore, the regulation of adhesion molecule expression involves a complex array of intracellular signaling pathways including mitogen-activated protein kinase (MAPKs), reactive oxygen species (ROS) and transcriptional factors. A better understanding of this might provide important insights into the prevention of AKI.

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Study Type : Observational
Estimated Enrollment : 50 participants
Observational Model: Cohort
Time Perspective: Prospective
Official Title: National Taiwan University Hospital Yu-Lin Branch
Study Start Date : February 2014
Estimated Primary Completion Date : December 2014
Estimated Study Completion Date : December 2014

Group/Cohort
Acute kidney injury
Acute kidney injury in ICU
Non acute kidney injury
Non acute kidney injury



Primary Outcome Measures :
  1. Renal function recovery (BUN, Cre) [ Time Frame: 1 month ]

Biospecimen Retention:   Samples Without DNA
Serum BUN, Cre, ICAM-1


Information from the National Library of Medicine

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Ages Eligible for Study:   20 Years to 90 Years   (Adult, Older Adult)
Sexes Eligible for Study:   All
Accepts Healthy Volunteers:   No
Sampling Method:   Probability Sample
Study Population
AKI in ICU
Criteria

Inclusion Criteria:

  • ICU patients

Exclusion Criteria:

  • Less than 20 years old

Information from the National Library of Medicine

To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor.

Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT02061566


Contacts
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Contact: Yu-Hsiang Chou, MD +886-972655372 chouyuhsiang@yahoo.com.tw

Locations
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Taiwan
National Taiwan University Hospital Not yet recruiting
Taipei, Taiwan, 100
Contact: Yu-Hsiang Chou, MD    +886-972655372    chouyuhsiang@yahoo.com.tw   
Sponsors and Collaborators
National Taiwan University Hospital
Investigators
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Principal Investigator: Yu-Hsiang Chou, MD NTUH Yun-Lin branch

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Responsible Party: National Taiwan University Hospital
ClinicalTrials.gov Identifier: NCT02061566     History of Changes
Other Study ID Numbers: 201310062RINA
First Posted: February 13, 2014    Key Record Dates
Last Update Posted: February 25, 2014
Last Verified: February 2014

Keywords provided by National Taiwan University Hospital:
Acute kidney injury

Additional relevant MeSH terms:
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Acute Kidney Injury
Renal Insufficiency
Kidney Diseases
Urologic Diseases