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Hypoalbuminemia in Dialysis Patients

Albumin normally comprises approximately 50% of total plasma protein mass. A reduced plasma concentration of this protein is the strongest independent risk factor for death in dialysis patients (1, 2). Because of its relatively low molecular weight and its great abundance, albumin provides the greatest contribution of plasma colloid osmotic pressure (oncotic pressure) of any plasma protein and thus contributes to retention of salt and water in the plasma compartment, supporting plasma volume and providing an important protection against edema. Albumin also binds and transports free fatty acids, which are otherwise toxic, and facilitates catabolism of lipoproteins by preventing the inhibition of lipoprotein lipase by released free fatty acids. In addition albumin binds other biologically relevant lipophilic molecules, such as steroid hormones, bilirubin, and divalent cations. Albumin is the principal binding protein for zinc. However, despite all of these important functions, albumin is not necessary for life. Individuals exist with hereditary analbuminemia and a strain of rat has also been well characterized that has albumin levels that approach zero. Although hyperlipidemia is present in both analbuminemic humans and rats, blood pressure is normal, as is plasma volume, and both are edema free. Rats with hereditary analbuminemia reproduce normally and, although they have a shortened life span, it is not at all certain that this is a direct result of analbuminemia. Furthermore, albumin levels are hardly ever reduced to less than 50% of normal serum levels in dialysis patients and excess mortality is observed when albumin levels are only slightly below 40 mg/mL (1, 2). Although hypoalbuminemia, or more specifically analbuminemia, elicits an increase in the plasma concentration of a number of high molecular weight proteins (3, 4), many of which have procoagulant properties, and increases blood viscosity, it is most