Cardiovascular disease (CVD) remains the major cause of morbidity and mortality in end-stage renal disease (ESRD) patients. As traditional risk factors cannot alone explain the unacceptable high prevalence and incidence of CVD in this population, inflammation (which is interrelated to insulin resistance, oxidative stress, wasting and endothelial dysfunction) has been suggested to be a significant contributor. Indeed, several different inflammatory biomarkers, such as high sensitivity C-reactive protein (hs-CRP), have been shown to independently predict mortality in ESRD patients. As CRP is so strongly associated with vascular disease it has been suggested that this hepatic-derived protein is not only a marker, but also a mediator of vascular disease. Indeed, recent in vitro data from studies on endothelial cells, monocytes-macrophages and smooth muscle cells support a direct role for CRP in atherogenesis. The causes of the highly prevalent state of inflammation in ESRD are multiple, including decreased renal function, volume overload, comorbidity and intercurrent clinical events, factors associated with the dialysis procedure and genetic factors. Recent evidence suggests that several cytokine DNA polymorphisms may affect the inflammatory state as well as outcome in ESRD patients. As interventions directed towards traditional risk factors have, so far, not proven to be very effective, controlled studies are needed to evaluate if various pharmacological as well as non-pharmacological anti-inflammatory treatment strategies, alone or in combination, may be an option to affect the unacceptable high cardiovascular mortality rate in this patient group.
