The Role of Blood Viscosity in Hemodialysis Patients

Abstract

Hemodialysis typically increases blood viscosity. Increased blood viscosity plays a role in accelerating atherothrombosis, in anemia, and in decreasing life expectancy in hemodialysis patients. Elevated blood viscosity increases the risk of thrombosis, decreases tissue perfusion, and increases systemic vascular resistance. Elevated blood viscosity also reduces the efficiency of hemodialysis, which can contribute to electrolyte abnormalities. Inefficient removal of protein-bound uremic toxins decreases the erythrocyte zeta potential, augmenting erythrocyte aggregation and low-shear blood viscosity. This contributes to accelerated atherothrombosis, which may be the most common cause of death in hemodialysis patients. The interaction of the systemic vascular resistance response and the renin-angiotensin-aldosterone system regulates blood viscosity even in renal failure patients. This regulation is accomplished in part by modulation of the hematocrit, which causes the anemia of renal failure. Erythropoiesis-stimulating agents interfere with this homeostatic response, increasing the risk of atherothrombosis and death. The change in intravascular volume caused by hemodialysis correlates with the change in blood viscosity, suggesting that viscometry may provide useful data in assessing a patient’s volume status. Capillary viscometry is the best method for measuring blood viscosity. On-site testing in a free-standing hemodialysis facility is feasible.