Abstract
Impaired hemostasis coexists with accelerated atherosclerosis in patients with chronic kidney disease (CKD). The elevated frequency of atherothrombotic events has been associated with endothelial dysfunction. The relative contribution of the uremic state and the impact of the renal replacement therapies have been often disregarded. Plasma markers of endothelial activation and damage were evaluated in three groups of patients with CKD: under conservative treatment (predialysis), on hemodialysis, and on peritoneal dialysis. Activation of p38 MAPK and the transcription factor NFκB was assessed in endothelial cell (EC) cultures exposed to pooled sera from each group of patients. Most of the markers evaluated (VCAM-1, ICAM-1, VWF, circulating endothelial cells) were significantly higher in CDK patients than in controls, being significantly more increased in the group of peritoneal dialysis patients. These results correlated with the activation of both p38 MAPK and NFκB in EC cells exposed to the same sera samples, and also to the peritoneal dialysis fluids. Hemodialysis did not further contribute to the endothelial damage induced by the uremic state observed in predialysis patients, probably due to the improved biocompatibility of the hemodialysis technique in recent years, resulting in lower cellular activation. However, peritoneal dialysis seemed to exert a significant proinflammatory effect on the endothelium that could be related to the high glucose concentrations and glucose degradation products present in the dialysis fluid. Although peritoneal dialysis has been traditionally considered a more physiological technique, our results raise some doubts with respect to inflammation and EC damage.
Highlights
Patients with chronic kidney disease (CKD) suffer from complex hemostasis disorders
We have investigated the relative contribution of uremia and renal replacement therapies (RRT), hemodialysis and peritoneal dialysis, to the development of endothelial damage in patients with CKD
The present study was focused to discern the contribution of uremia and the RRT to the development of endothelial activation and damage
Summary
Patients with chronic kidney disease (CKD) suffer from complex hemostasis disorders Both a bleeding tendency and an increased risk of accelerated atherosclerosis, with a high incidence of cardiovascular death, have been described to coexist [1]. In patients with CKD, the progression of atherothrombosis is accelerated [14], causing early cardiovascular complications [15] In this regard, mortality from cardiovascular disease is nearly tenfold higher in patients with end-stage renal disease (ESRD) on dialysis than in the general population (US Renal Data System, USRDS 2009 Annual Data Report). Mortality from cardiovascular disease is nearly tenfold higher in patients with end-stage renal disease (ESRD) on dialysis than in the general population (US Renal Data System, USRDS 2009 Annual Data Report) This clinical situation cannot be fully explained by an increased prevalence of traditional cardiovascular risk factors such as hypertension, diabetes, hyperlipidemia or smoking, in ESRD [16]. An enhanced cardiovascular risk has been reported in patients with CKD not on dialysis [17]
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