Hypoalbuminemia in heart failure: pathophysiology, clinical implications, and management strategies.

Abstract

Hypoalbuminemia is commonly seen in patients with heart failure and is associated with worse outcomes. Multiple pathophysiologic mechanisms can contribute to low albumin levels in heart failure patients, such as malnutrition, hepatic congestion, inflammation, and protein-losing enteropathy. Hypoalbuminemia can exacerbate heart failure symptoms and contributes to pulmonary edema by reducing plasma oncotic pressure, thereby favoring fluid movement into the interstitial and alveolar spaces. In this sense, albumin supplementation has been used in clinical practice to stimulate diuresis. However, evidence regarding its efficacy remains controversial. Routine albumin use does not appear to improve outcomes and should not be adopted broadly. Instead, it may be considered selectively in those with refractory edema or ascites despite maximal diuretic therapy and in whom hypoalbuminemia is profound. While proper oral nutrition has clearly shown better outcomes in malnourished heart failure patients, no clear guidelines about the use of intravenous albumin therapy are currently available to guide this practice. This article aims to review the pathophysiology of hypoalbuminemia in heart failure and the current available evidence on the therapeutic role of albumin infusion.