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A Journal on Angiology

Official Journal of the International Union of Angiology, the International Union of Phlebology and the Central European Vascular Forum
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International Angiology 2016 Apr 15

language: English

Effect of erythropoietin stimulating agents on vascular endothelial growth factor levels in patients with end stage renal disease

Jennifer L. SALUK 1, Vinod BANSAL 2, Debra HOPPENSTEADT 3, Daneyal SYED 3, Schuharazad ABRO 3, Jawed FAREED 3

1 Stritch School of Medicine, Loyola University of Chicago, Maywood, USA; 2 Nephrology, Department of Internal Medicine, Loyola University Medical Centre, Maywood, IL, USA; 3 Hemostasis and Thrombosis, Department of Pathology, Loyola University Medical Centre, Maywood, IL, USA


BACKGROUND: End stage renal disease (ESRD) is a debilitating disease that not only impacts quality of life, but also increases the risk of cardiovascular disease, stroke, and overall mortality. By improving our understanding of the molecular patterns seen in progression of chronic renal disease (CRD), we may be able to slow down and possibly even prevent progression renal failure. The vascular endothelial growth factor (VEGF) has been implicated as a major contributor to CRD disease progression, thus our aim was to profile the VEGF levels in patients with ESRD and to determine the effects of the erythropoietin stimulating agents (ESAs).
METHODS: Under institution review board (IRB) approval, plasma samples were collected from 77 patients prior to hemodialysis and heparin administration. Normal human plasma samples (female & male, 18-35 years old) were purchased from George King Biomedical Inc (Overland Park, KS). All samples were stored at -80°C. Inflammatory biochips were purchased from RANDOX (Co. Antrim, Northern Ireland) to test VEGF on 77 ESRD and 48 normal samples.
RESULTS: The VEGF was significantly elevated in ESRD vs. normal (P<0.0001), ESRD+ESA vs. normal (P<0.0001), and ESRD-ESA vs. normal (P<0.0001). No difference was seen between ESRD+ESA and ESRD-ESA. Hemoglobin and free iron were significantly elevated in ESRD- ESA compared to ESRD+ESA (PHemoglobin=0.0007, PIron<0.0001).
CONCLUSIONS: Our finding that VEGF was significantly elevated in ESRD vs. normal, aligns with the literature and suggests that VEGF may in fact play a key role in CRD progression. However, further studies to evaluate VEGF isomer levels are needed. While we saw lack of difference in VEGF levels between ESRD+ESA and ESRD-ESA, this may be due to the treatment algorithm used. Further investigation is warranted to determine whether the ESAs and hemoglobin levels show any influence on or crosstalk with the VEGF levels.

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