Haemodialysis, atherosclerosis and inflammation-identifying molecular mechanisms of chronic vascular disease in ESDR patients.

Abstract

Patients suffering from end-stage renal disease (ESRD) require haemodialysis (HD) to substitute the lack of excretory kidney function. Novel techniques and improved material have led to dialysis protocols which are able to sustain a patient’s life for years, and even decades. However, despite all these improvements in the dialysis regimen, many unsolved clinical problems remain. A major problem is the excess morbidity and mortality of dialysis patients due to cardiovascular disease. The 5-year survival rate on stable HD is ;35% in an average urban ESRD patient population w1x. Cardiovascular morbidity due to accelerated atherosclerosis determines the prognosis of haemodialysed patients w2,3x. The cause of the enhanced occurrence of atherosclerosis in dialysis patients is unclear, although it is obvious that various risk factors are involved. Elevated blood pressure, a high rate of diabetes mellitus, increased plasma lipid concentrations, ‘uraemic toxins’, etc. play a role in the pathogenesis of the accelerated atherosclerosis in dialysis patients. Recently, the inflammatory nature of chronic vascular disease has received much attention and it has been postulated that haemodialysis may contribute to the inflammatory vascular response in these patients.