Abstract
Hypoalbuminemia is common in patients with end-stage renal disease (ESRD). It is caused by a combination of a reduced synthesis and an increased degradation of albumin. The altered albumin homeostasis in ESRD patients is caused by a systemic inflammatory state which correlates closely with mortality. Hypoalbuminemia is a strong predictor of an adverse prognosis, but it is not a pathogenic factor in itself. In critically ill patients in intensive care units, the intravenous administration of human serum albumin generally does not improve prognosis. In contrast, in hypoalbuminemic dialysis patients with volume overload and a reduced effective arterial volume the administration of albumin is based on the pathophysiological concept of increasing intravascular oncotic pressure to transfer extravascular fluid into the intravascular compartment for ultrafiltration in order to mobilize edema fluid.