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Hypoalbuminaemia refers to a reduced blood concentration of albumin, one of the major plasma proteins which is synthesised in the liver. Albumin has multiple physiological functions including exertion of 75% of the total plasma oncotic pressure (to prevent leakage of fluid into body cavities and the interstitium), carriage of drugs and hormones in the blood (particularly thyroid and reproductive hormones and non-steroidal anti-inflammatory drugs) and buffering of blood pH changes. Albumin has a circulating half-life of 17-19 days and its normal serum concentration is 25-40 g/l.

Causes of Hypoalbuminaemia

The synthesis of albumin may be reduced or it may be lost in greater quantities than normal:

Reduced synthesis of albumin

  • Severe malnutrition resulting in the inability to synthesise sufficient albumin, also known as protein energy malnutrition.
  • Elaboration of an acute phase response, in which the production of positive acute phase proteins (such as globulins and c reactive protein) is favoured at the expense of negative acute phase proteins like albumin and transferrin. Globulins will be elevated in this response, with a reduced albumin: globulin ratio.
  • Severe hepatic insufficiency, as in chronic liver failure or with congenital porto-systemic shunts.

Increased loss of albumin

  • Severe exudates that contain large quantities of protein may deplete the plasma proteins:
    • Dermal protein loss after severe thermal or chemical burns.
    • Septic peritonitis involving copious amounts of exudative peritoneal fluid.
  • Protein-losing enteropathy (PLE) caused by inflammatory bowel disease, lymphangiectasia or alimentary lymphoma. Globulins and, in severe cases, whole blood are lost with albumin in this condition.
  • Protein-losing nephropathy (PLN) caused by primary glomerulopathy, glomerulonephritis or amyloidosis. Albumin, having a smaller molecular weight, is lost in great excess of globulin. Severe PLN results in Nephrotic Syndrome characterised by severe hypoproteinaemia, hypercholesterolaemia, ascites, hydrothorax and subcutaneous oedema.
  • Acute haemorrhage followed by autotransfusion (movement of fluid into the circulation from the interstitium) will result in dilution of the remaining plasma proteins.

Apparent hypoalbuminaemia may occur in overhydrated or hypervolaemic animals suffering from primary (psychogenic) polydipsia or which have received intra-venous fluid therapy.

Consequences of Hypoalbuminaemia

Albumin is the major plasma protein contributing to the maintenance of plasma oncotic pressure (also known as colloid osmotic pressure). This force opposes hydrostatic pressure and prevents the loss of intravascular fluid into body cavities and the interstitial space. Hypoalbuminaemia may therefore lead to the following conditions when the concentration of albumin falls below 10-15 g/l:

  • Ascites and hydrothorax composed of transudate fluid.
  • Pericardial effusion composed of transudate fluid and causing cardiac tamponade.
  • Pulmonary oedema which, together with hydrothorax, will cause dyspnoea.
  • Subcutaneous oedema is an unusual finding, even in severe hypoalbuminaemia.
  • Hypotension due to an inability to maintain an adequate intravascular volume.
  • Reduction in total calcium concentration (as 40-50% is bound to plasma protein) but ionised calcium concentration may not be altered.


Total serum protein concentration can be estimated by refractometry but this technique does not differentiate albumin from the plasma globulins. This is important because, in some chronic inflammatory liver diseases, albumin may be reduced by hepatic insufficiency while total protein concentration may remain normal due to the production of globulins in the inflammatory process.

Ideally, albumin and globulin concentrations should be measured individually so that an albumin: globulin ratio can be calculated.

Urinalysis and haematological and biochemical blood profiles may identify further abnormalities relating to the underlying cause of the hypoalbuminaemia.


Any underlying cause should be treated but, in animals showing clinical signs related to hypoalbuminaemia, consideration should be given to plasma transfusions or to administration of recombinant human albumin. Effusions should only be drained if they are causing serious clinical signs as this procedure will deplete protein reserves even further.


Prognosis is dependent on the underlying cause of the disease.

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