Red Blood Cell Distribution Width as a Marker of Contrast Induced Nephropathy in Patients With Coronary Intervention
NCT ID: NCT03164681
Last Updated: 2017-05-24
Study Results
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Basic Information
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UNKNOWN
126 participants
OBSERVATIONAL
2017-12-01
2018-12-30
Brief Summary
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Detailed Description
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The development of Contrast Induced Nephropathy after Percutaneous Coronary Intervention is associated with poor clinical outcomes including prolonged hospitalization, increased costs, increased rates of end-stage renal failure, myocardial infarction, repeat revascularization, and short- and long-term mortality.
Contrast Induced Nephropathy follows decreased renal perfusion and administration of nephrotoxic medications as the third most common cause of renal insufficiency during hospitalization.
Patients with acute coronary syndrome have a 3-fold higher risk of developing Contrast Induced Nephropathy .Therefore ,predicting contrast nephropathy and initiating therapeutic preventive strategies are very important.
Red Blood Cell Distribution Width is a quantitive marker of the variability on size of erythrocyte.
It is a routine assay of Complete Blood Count that doesn't require an additional cost, that is calculated by dividing the standard deviation of the mean cell size by the Mean Corpuscular Volume of the red cells and multiplying by 100 to convert to a percentage.
Normal range of Red Blood Cell Distribution Width 11-16%. Increased Red Blood Cell Distribution Width means increased variability in red blood cell size owing to ineffective erythrocyte production, which is associated with indices of inflammation and pro-inflammatory cytokines such as interleukin-6 .
On the other hand, suggested mechanisms underlying Contrast Induced Nephropathy include cytotoxic effects, factors that affect renal hemodynamic, and regional hypoxia.
Conditions
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Study Design
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COHORT
PROSPECTIVE
Eligibility Criteria
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Inclusion Criteria
Exclusion Criteria
2. Patient known allergy to contrast agents.
3. Left ventricular ejection fraction below 30%.
4. Presence of infection
5. A recent history of contrast administration in the previous month.
6. Patient known to have thyroid disease.
7. History of malignancy.
8. Patient known to have Autoimmune disease.
9. Decompensated liver cirrhosis
10. Cardiogenic shock.
11. Anemia
ALL
No
Sponsors
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Assiut University
OTHER
Responsible Party
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Sherly Boshra
Principal Investigator
Principal Investigators
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sherly boshra
Role: PRINCIPAL_INVESTIGATOR
Assiut University
Central Contacts
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References
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Mehran R, Nikolsky E. Contrast-induced nephropathy: definition, epidemiology, and patients at risk. Kidney Int Suppl. 2006 Apr;(100):S11-5. doi: 10.1038/sj.ki.5000368.
Marenzi G, Lauri G, Assanelli E, Campodonico J, De Metrio M, Marana I, Grazi M, Veglia F, Bartorelli AL. Contrast-induced nephropathy in patients undergoing primary angioplasty for acute myocardial infarction. J Am Coll Cardiol. 2004 Nov 2;44(9):1780-5. doi: 10.1016/j.jacc.2004.07.043.
McCullough PA. Contrast-induced acute kidney injury. J Am Coll Cardiol. 2008 Apr 15;51(15):1419-28. doi: 10.1016/j.jacc.2007.12.035.
Bartholomew BA, Harjai KJ, Dukkipati S, Boura JA, Yerkey MW, Glazier S, Grines CL, O'Neill WW. Impact of nephropathy after percutaneous coronary intervention and a method for risk stratification. Am J Cardiol. 2004 Jun 15;93(12):1515-9. doi: 10.1016/j.amjcard.2004.03.008.
Nash K, Hafeez A, Hou S. Hospital-acquired renal insufficiency. Am J Kidney Dis. 2002 May;39(5):930-6. doi: 10.1053/ajkd.2002.32766.
Tepel M, Aspelin P, Lameire N. Contrast-induced nephropathy: a clinical and evidence-based approach. Circulation. 2006 Apr 11;113(14):1799-806. doi: 10.1161/CIRCULATIONAHA.105.595090. No abstract available.
Seeliger E, Sendeski M, Rihal CS, Persson PB. Contrast-induced kidney injury: mechanisms, risk factors, and prevention. Eur Heart J. 2012 Aug;33(16):2007-15. doi: 10.1093/eurheartj/ehr494. Epub 2012 Jan 19.
Other Identifiers
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RDWCIN
Identifier Type: -
Identifier Source: org_study_id
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