Purpose of review Albumin plays a central role in maintaining circulatory and endothelial homeostasis through its oncotic and nononcotic effects. In cirrhosis, reduced concentration and impaired function of albumin contribute to circulatory derangements, renal dysfunction, and infection risk. While albumin is firmly established in certain settings such as spontaneous bacterial peritonitis (SBP), hepatorenal syndrome (HRS), and large-volume paracentesis (LVP), its broader use in cirrhosis remains controversial and incompletely defined. We aim to integrate up to date guidance on the use of albumin in cirrhosis, and to highlight areas where evidence remains limited or evolving. Recent findings Evidence from randomized trials and meta-analyses highlights both established and emerging roles of albumin in cirrhosis. Albumin has demonstrated clear benefit after LVP, where it reduces postprocedural circulatory dysfunction, renal impairment, and hyponatremia compared with other plasma expanders. In HRS, albumin serves as an indispensable therapeutic backbone, enhancing the efficacy of vasoconstrictors and improving rates of renal reversal, yet its independent role remains incompletely defined. In SBP, co-administration of albumin with antibiotics reduces renal failure and improves short-term survival, establishing it as standard of care. In acute kidney injury (AKI) outside of HRS, current guidelines recommend the use of albumin as part of an initial volume challenge in many forms of AKI to aid diagnosis and potentially promote renal recovery, although the timing of its use differs among guidelines. Summary Albumin is a cornerstone therapy in the management of decompensated cirrhosis and its clinical complications. While its role is well defined in HRS, SBP, and post-LVP, higher-quality evidence is needed to refine its use in other settings, particularly in AKI.
Besir et al. (Fri,) studied this question.
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