Albumin is an acute phase reactant that is known to be influenced by many factors including the presence of an underlying inflammatory process. Inflammation was shown to reduce albumin levels irrespective of the patient's nutritional state [1], and albumin has thus been considered a negative acute-phase reactant. Among the reasons for reduced albumin levels during acute and chronic inflammatory states is the increased albumin degradation from the high catabolic rate, in addition to its transudation to the extravascular space from increased capillary permeability (e.g.
