alexa Serum Profiles of Pentraxin-3 and High Sensitivity C - Reactive Protein in Patients with Chronic Kidney Disease Treated with or without Hemodialysis | OMICS International | Abstract
ISSN: 2161-0959

Journal of Nephrology & Therapeutics
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Research Article

Serum Profiles of Pentraxin-3 and High Sensitivity C - Reactive Protein in Patients with Chronic Kidney Disease Treated with or without Hemodialysis

EL-Attar HA1*, Abaza MM1, Gaber EW2 and EL-sharkawy RM1

1Chemical Pathology Department, Medical Research Institute, University of Alexandria, Israel

2Internal Medicine Department, Medical Research Institute, University of Alexandria, Israel

*Corresponding Author:
EL-Attar HA
Medical Research Institute
University of Alexandria, Israel
Tel: +201020244286
E-mail: [email protected]

Received Date: January 28, 2017; Accepted Date: February 4, 2017; Published Date: February 10, 2017

Citation: EL-Attar HA, Abaza MM, Gaber EW, EL-sharkawy RM (2017) Serum Profiles of Pentraxin-3 and High Sensitivity C - Reactive Protein in Patients with Chronic Kidney Disease Treated with or without Hemodialysis. J Nephrol Ther 7: 286. doi:10.4172/2161-0959.1000286

Copyright: © 2017 EL-Attar HA, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Background: The first cloned long pentraxin is Pentraxin 3(PTX3) and C-reactive protein is a human short pentraxin. Pentraxin 3 has a bigger molecular size (40.6 kDA) compared to CRP (21.5 kDa).The long PTX3 is produced by diverse cell types in response to primary inflammatory signals and specific neutrophil granules store PTX3. Aim: Evaluate serum levels of long pentraxin 3 and high sensitivity C-reactive protein in patients with chronic kidney disease treated with or without hemodialysis. The study included 75 subjects, 25 heathy controls (group 1), 50 patients without cardiovascular disease subdivided into: 25 patients with chronic kidney disease (CKD) on conservative therapy (group 2a) and 25CKD patients on maintenance hemodialysis (group 2b). To all studied subjects the following was done: electocardiography, carotid intima media thickness, fasting serum glucose, renal, liver and lipid profiles, high- sensitivity C-reactive protein (hsCRP) and PTX3by ELISA. Results: There was a significant decrease in the mean levels of albumin in all the studied chronic renal failure patients when compared to controls. Hypoalbuminemia is due to malnutrition and inflammation in CKD patients. There was a significant increase in hsCRP in patients on hemodialysis therapy when compared to both controls and patients on non-dialytic therapy. The circulating value of CRP reflects ongoing inflammation and/or tissue damage. There was a significant increase in PTX3 in patients on hemodialysis therapy as compared to controls. PTX3 levels may directly reflect the inflammatory status. Since a state of persistant low-grade inflammation is a common feature in hemodialysis patients so PTX3 increased in such patients. There were no correlations between PTX3 and hsCRP in the studied groups. By drawing the ROC curve for hsCRP and PTX3 in patients on non-dialytic therapy (group 2a), the area under the curve was 0.545 (p=0.594) and 0.653 (p=0.073) respectively. In patients on hemodialysis therapy (group 2b), the area under the curve was 0.735 (p=0.006) for hsCRP and 0.765 (p=0.002) for PTX3. By using the best cut off values, it was found that high sensitivity C-reactive protein showed a better specificity and positive predictive value than PTX3 while PTX3 showed a better sensitivity than hsCRP in the studied two groups of patients. Conclusion: It could be concluded that using both hsCRP and PTX3 complement each other to give better specificity and sensitivity as predictors of inflammation in chronic kidney disease patients. Recommendation: Study of PTX3 and hsCRP on a large number of chronic kidney disease patients with cardiovascular disease.

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