SP117
ENDOCAN AS A BIOMARKER OF ENDOTHELIAL FUNCTION IN END STAGE RENAL DISEASE

Introduction and Aims: Endocan also described as endothelial cell specific molecule (ESM1) is a proteoglycan of 50kda which is highly upregulated in various vascular diseases. Endocan binds CD11a / CD18 integrin on human leukocyte. Pro-inflammatory mediators such as TNFalpha and proantiogenic molecules such as VEGF or FGF 2 stimulate the formation of this mediator. Elevated blood levels of endocan have been reported in patients with cancer (lung, kidney, blood), severe sepsis, and post-transplantation veno-occlusive disease. The purpose of this study is to measure endocan in ESRD patients to demonstrate its relevance to this disease.

Methods: Citrated plasma samples were collected from 85 patients who were on maintenance hemodialysis in the dialysis clinic at Loyola University Chicago Hospital. The control group represents 50 normal, drug free individuals. Endocan levels were measured in these plasma samples using a commercially available ELISA method (Lunginnov,Paris, France). VEGF and FGF 2 levels were also measured using commercially available ELISA methods (R&D, Minneapolis, Minnesota).

Results: Endocan levels were found to be significantly higher (p=<0.05) in the ESRD patients (2.6 ± 1.3ng/ml) with a wide range (0.9 ± 14.7 ng/ml) in contrast to normal (1.8 ± 0.6ng/ml) with a narrower range of (1.3 ± 3.4ng/ml). Of the 85 patients, 10 showed greater than 5 ng/ml of this biomarker. Both the VEGF level and FGF 2 levels were also elevated (2-5 folds) in the ESRD group in comparison to the normal. There was a poor correlation (r=<0.3) between the elevation of endocan with either VEGF and FGF 2.

Conclusions: Consistent with earlier reports endocan is elevated in various diseases with endothelial dysfunction. These studies suggest that this biomarker may be a useful prognostic indicator for ESRD. Contrary to the earlier reports the observed poor correlation between endocan and VEGF / FGF 2 may suggest independent regulation of endocan through other mechanisms. This data warrants additional studies to validate the relevance of this marker with the pathogenesis of ESRD.