Albumin is an interface between blood plasma and cell membrane, and not just a sponge

Abstract

Albumin is the most abundant protein in blood plasma and acts as a carrier for many circulating molecules. Hypoalbuminemia, mostly caused by either renal or liver disease or malnutrition, can perturb vascular homeostasis and is involved in development of multiple diseases. Here we review four functions of albumin and the consequences of hypoalbuminemia on vascular homeostasis. (i) Albumin is the main determinant of plasma colloid-osmotic pressure. Hypoalbuminemia was therefore thought to be the main mechanism for edema in nephrotic syndrome, however experimental studies showed that intrarenal mechanisms rather than hypoalbuminemia determine formation and in particular maintenance of edema. (ii) Albumin functions as an interface between lysophosphatidylcholine (LPC) and circulating factors (lipoproteins and erythrocytes) and the endothelium. Consequently, hypoalbuminemia results in higher LPC levels in lipoproteins and erythrocyte membrane, thereby increasing atherosclerotic properties of low-density lipoprotein and blood viscosity, respectively. Furthermore, albumin dose-dependently restores LPC-induced inhibition of vasodilation. (iii) Hypoalbuminemia impacts on vascular nitric oxide (NO) signaling by directly increasing NO-production in endothelial cells, leading to reduced NO-sensitivity of vascular smooth muscle cells. (iv) Lastly, albumin binds free fatty acids (FFA). FFA can induce vascular smooth muscle cell apoptosis, uncouple endothelial NO synthase and decrease endothelium-dependent vasodilation. Unbound FFA can increase formation of reactive oxygen species by mitochondrial uncoupling in multiple cell types and induce hypertriglyceridemia in nephrotic syndrome. In conclusion, albumin acts as an interface in the circulation and hypoalbuminemia impairs multiple aspects of vascular function which may underlie the association of hypoalbuminemia with adverse outcomes. However, hypoalbuminemia is not key to edema in nephrotic syndrome. These insights have therapeutic implications.

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