Role of Hypoalbuminemia in the Genesis of Cardiovascular Disease in Dialysis Patients

Abstract

Our objective was to review the articles about the association between hypoalbuminemia and atherosclerotic or thrombotic cardiovascular disease (CVD) and to look for possible explanations for the role of hypoalbuminemia. Increased incidences of CVD were reported in patients with hypoalbuminemia owing to renal or other diseases. Hypoalbuminemia increases plasma levels of lipoprotein(a), fibrinogen, and arachidonic acid metabolites; it also increases platelet aggregability and blood viscosity, all of which may contribute to the development of CVD. This cause-effect association is thought to be “dependent.” Changes in atherogenic lipoproteins or lipids, such as LDL cholesterol, triglycerides, and apolipoprotein B, are controversial in hypoalbuminemic dialysis patients, possibly because coexistent malnutrition and volume status can affect both albumin and lipids. In our recent study, there was a negative correlation between serum albumin and C-reactive protein, D-dimer (an index of intravascular thrombogenesis), and von Willebrand factor (a marker for endothelial cell injury), but infusion of albumin did not affect the level of these parameters, which suggests that the correlations may be an effect-effect association by a confounding variable, such as inflammation. In conclusion, hypoalbuminemia is associated with cardiovascular disease via two pathways: one, a “dependent” cause-effect association; the other, an effect-effect association.