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Editorials |

Another Nail in Albumin’s Coffin

Lewis J. Kaplan, MD, FCCP
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New Haven, CT

Correspondence to: Lewis J. Kaplan, MD, FCCP, Associate Professor of Surgery and Director, Surgical ICU and Surgical Critical Care Fellowship, Yale University School of Medicine, 330 Cedar St, BB-310, New Haven, CT 06520; e-mail: Lewis.Kaplan@yale.edu



Chest. 2007;131(5):1276-1277. doi:10.1378/chest.07-0313
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In this issue of CHEST (see page 1295),1 one finds another important investigation that addresses one of the fundamental tenets of acid-base physiology: the role of albumin as a buffer base. Few therapies have entrenched themselves in medicine with the same tenacity as albumin administration. According to conventional wisdom, albumin functions as a buffer base and should, therefore, blunt the acidosis generated by increases in Pco2. In an elegantly designed investigation, Gomez and colleagues,1 varied Pco2 in rodents with either normal albumin, hypoalbuminemia, or analbuminemia. If albumin serves this central buffer base role, then for a given increase in Pco2, the effects of acidosis (principally hypotension) should be proportional to the decrement in albumin from normal. Despite identifying a decreased buffer capacity in the hypoalbuminemic and analbuminemic rats, no such BP effect was observed. This observation casts further doubts onto the time-honored practice of albumin administration in the critically ill, as one can no longer support such a practice on the basis of acidosis buffering in the setting of permissive hypercapnia for lung injury or ARDS.2

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