Circulating E‐selectin as a risk marker in patients with end‐stage renal disease

. Background.  E‐selectin is a key adhesion molecule which plays a fundamental role in endothelial progenitor cell‐dependent reparative mechanisms in experimental ischaemia and it serves to anchor leucocytes to the endothelium in inflammatory processes. Inflammation is one of the strongest risk fact...

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Veröffentlicht in:Journal of internal medicine 2007-10, Vol.262 (4), p.479-487
Hauptverfasser: Malatino, L. S., Stancanelli, B., Cataliotti, A., Bellanuova, I., Fatuzzo, P., Rapisarda, F., Leonardis, D., Tripepi, G., Mallamaci, F., Zoccali, C.
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Sprache:eng
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Zusammenfassung:. Background.  E‐selectin is a key adhesion molecule which plays a fundamental role in endothelial progenitor cell‐dependent reparative mechanisms in experimental ischaemia and it serves to anchor leucocytes to the endothelium in inflammatory processes. Inflammation is one of the strongest risk factors for death and cardiovascular (CV) events in end‐stage renal disease (ESRD). Objective.  The objective of the current study was to evaluate whether E‐selectin is a useful biomarker of clinical outcome in ESRD patients. We tested the prediction power of circulating E‐selectin for mortality and CV events in a cohort of 265 ESRD patients. Results.  During the follow‐up, 59 patients died and 58 had CV events. All‐cause mortality was inversely related to serum E‐selectin, the risk of death being the lowest in patients in the third E‐selectin tertile (HR: 1, reference group), intermediate in those in the second tertile (HR: 1.30) and the highest in patients in the first tertile (HR: 2.02, P = 0.01). Similarly, the risk of fatal and nonfatal CV events followed an inverse pattern being lowest in the third tertile (reference group) and highest in the first tertile (HR: 1.73, P = 0.03). The prediction power of E‐selectin for death and CV events was confirmed in a Cox regression analysis where E‐selectin emerged as an inverse predictor of these outcomes, particularly so in patients with severe inflammation. Conclusions.  These data are in keeping with the hypothesis that in systemic inflammation altered E‐selectin shedding may play a role in arterial damage and implicates this adhesion molecule in atherosclerotic complications in a high‐risk condition like ESRD.
ISSN:0954-6820
1365-2796
DOI:10.1111/j.1365-2796.2007.01841.x