Upregulation of surrogate markers of inflammation and thrombogenesis in patients with ESRD: pathophysiologic and therapeutic implications.

Patients with end-stage renal disease (ESRD) undergoing regular hemodialysis have high annual mortality rate of around 15%. The most predominant cause of death is cardiovascular, which is not entirely explainable with conventional cardiac risk factors present in these patients. It has been postulated that ESRD is a chronic inflammatory and hypercoagulable condition with marked elevation of several markers that may explain this high mortality. In the current study, patients with ESRD on a stable regimen of hemodialysis were studied for the inflammatory and thrombogenesis markers to explain this phenomenon. The parameters studied were of thrombogenesis-thrombin-antithrombin III complex (TAT), prothrombin fragment (F1.2), D-dimer, and fibrinopeptide A (FPA) and inflammation-CD40 ligand, myeloperoxidase (MPO), tumor necrosis factor α (TNF-α), monocyte chemotactic protein-1 (MCP-1), and nitric oxide (NO), and compared to control group comprised of 100 healthy volunteers. Our study shows that ESRD patients exhibit activation of the coagulation and inflammatory processes.