Correlation of Fibroblast Growth Factor 23 with Markers of Inflammation and Endothelial Dysfunction in End-Stage Renal Disease and Type 2 Diabetes Patients on Peritoneal DialysisRuchi Singh, Sudha P Chennasamudram, Sudip Sheth and Tetyana L Vasylyeva*
Texas Tech University Health Sciences Center, Amarillo, Texas, USA
- *Corresponding Author:
- Tetyana L Vasylyeva
Texas Tech Health Sciences Center
Pediatrics, 1400 S. Coulter, Amarillo, TX 79106, USA
E-mail: [email protected]
Received date: April 16, 2014; Accepted date: May 16, 2014; Published date: May 20, 2014
Citation: Singh R, Chennasamudram SP, Sheth S, Vasylyeva TL (2014) Correlation of Fibroblast Growth Factor 23 with Markers of Inflammation and Endothelial Dysfunction in End-Stage Renal Disease and Type 2 Diabetes Patients on Peritoneal Dialysis. J Diabetes Metab 5:371. doi: 10.4172/2155-6156.1000371
Copyright: © 2014 Singh R, 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.
Objective: This study was design to evaluate the correlation between FGF-23 and other cardiovascular risk factors (markers of endothelial dysfunction and inflammation) in ESRD patients with T2DM on PD.
Method: Sixty serum samples collected (four times, at weeks 0, 8, 10, and 18) from 15 patients with Type 2 Diabetes (T2DM) and ESRD on PD were analysed to study the relationship between the levels of FGF-23 and markers of endothelial dysfunction and inflammation. ELISA kits were used to quantitate Endothelin-1 (ET-1), soluble vascular adhesion molecule, Plasminogen Activator Inhibitor-1 (PAI-1), FGF-23, C-reactive protein, Interleukin-6 (IL-6), Tumor Necrosis Factor Alpha (TNF-α) and cluster of differentiation 146 (CD 146). The association between FGF-23, mineral metabolites, and markers of inflammation were analyzed using Spearman correlations. Linear regression models were used to examine the univariate and multivariate adjusted associations between FGF-23 as primary exposure and individual inflammatory markers [including IL-6, PAI-1 and CD146] as the dependent variables. Multivariate analyses were adjusted for factors associated with mineral metabolism such as serum phosphate, Ca×PO4 product, and LDL concentration. Two-sided p values<0.05 were considered statistically significant.
Result: FGF-23 was positively correlated with phosphate (r=0.57; p<0.0001) and Ca×PO4 product (r=0.61; p<0.0001). FGF-23 showed the strongest correlation with IL-6 (r=0.32; p<0.05), PAI-1 (r=0.21; p<0.05) and CD 146 (r=0.29; p<0.05). In univariate and multivariate regression analysis, FGF-23 was significantly associated with IL-6, PAI-1, and CD 146. These results were qualitatively unchanged in the model that was further adjusted for Ca×PO4 product, serum phosphate, and LDL.
Conclusion: Our results indicate that FGF-23 impacts the cardiovascular health of T2DM patients on PD through mechanisms, which are independent from phosphate levels and linked directly to inflammation and endothelial dysfunction.