IntroductionHypoalbuminaemia is a result of a number of influencesduring the natural history of disease. It is, therefore, apathophysiological marker and not a disease entity forwhich there is any specific treatment. Indeed those withcongenital analbuminaemia may be symptom-free andremain in perfect health (1, 2). Treatment, therefore, isthat of the underlying condition causing hypoalbumi-naemia or associated with it.Hypoalbuminaemia is not a specific nutritionalmarker, since it is possible to die of starvation with anormal serum albumin. On the other hand, if disease ispresent, the serum albumin concentration falls inproportion to the severity and time-span of that disease.It is not surprising, therefore, that there is a goodcorrelation between a low serum albumin and pooreroutcome (3), as shown in many of the so-called‘predictive nutritional indices’ (4–7). This does notimply that simply raising the serum albumin concentra-tion by albumin infusion will improve outcome. Indeedthe opposite may be true (8, 9). Addressing the causes ofand associations with hypoalbuminaemia is more logicaland successful. We shall therefore consider the treat-ment of hypoalbuminaemia in relation to its three maincauses, i.e. inflammation with redistribution, dilution bycrystalloids and changes in metabolism. We shall alsoconsider the problem of its association with a lowplasma volume in the post-acute phase of illness.Inflammation: albumin distributionIn health, there is a continual flux of albumin whichleaks slowly from the intravascular space across thecapillary membrane and is returned via the lymphaticsystem (10). This flux is ten times the rate of albuminsynthesis, and the total intravascular albumin is ex-changed every one to two days. The cytokine responseto injury, infection, inflammation or cancer increasesvascular permeability and accelerates the escape rate ofalbumin from the circulation (11–13), causing not onlylocal swelling, wheal and flare, but also a generalizedredistribution of albumin from the circulation to theinterstitial space. These changes also contribute to thedrop in circulating volume and the shock associatedwith acute trauma and sepsis. They also explain whyacute changes in albumin distribution have a far morerapid and profound effect on its concentration than anyalteration in synthesis or catabolism.It has been argued, not unreasonably, that the use ofalbumin solutions for the treatment of circulatoryhypovolaermia in acute illness is unjustified because ofits rapid leakage from the circulation. Plasma substi-tutes, which normally have a shorter half-life thanalbumin in the circulation, may have a longer half-life inacute illness and injury (14), and are generally to bepreferred for volume expansion in the acute phase.Alternatives are crystalloid or a combination of crystal-loid and colloid. The relative effectiveness of these usedseparately or in combination is much debated (8, 15–19)and outside the scope of this paper. The primaryconcern is to maintain the intravascular volume andpreserve the circulation, rather than to address thealbumin concentration (20). On the other hand,profound falls in albumin concentration, as Guytonshowed (21), may predispose to systemic and pulmonaryoedema unless excessive administration of salt and wateris avoided. Albumin solutions are still in widespread usein paediatrics for the treatment of conditions such asshock in meningococcal septicaemia and have provedeffective in some adult conditions, including sponta-neous bacterial peritonitis associated with liver cirrhosis(22). This area, therefore, requires much more carefulthought and study before strong conclusions can bereached.Treatment of redistributional hypoalbuminaemia inacute inflammatory conditions or in malignant diseaseshould therefore be directed to its cause, i.e. draining theabscess, treating with antibiotics, removing the cancer,or using anti-inflammatory drugs. Once the cause hasbeen resolved, the albumin concentration will return tonormal with time and adequate nutrition.