Albumin is the major determinant of oncotic or colloidal osmotic pressure, the force that holds fluids within the vascular compartment. Most of the important osmotically-active particles in the bloodstream
(such as sodium, urea and glucose) are relatively small, and pass freely between the vascular and interstitial compartments,
the body's two major extracellular fluid compartments. Albumin, in contrast, is too large to pass freely through the vascular
endothelium, and remains within the bloodstream. The oncotic pressure within vessels due to the presence of albumin is the
major force holding fluid within the vascular compartment, although other plasma proteins such as globulins also have some
oncotic force. Hypoalbuminemia leads to a decrease in plasma oncotic pressure, which can eventually lead to a leakage of fluid
out from the vascular compartment.
Clinical Signs of Hypoalbuminemia
The classic clinical manifestations of hypoalbuminemia include peripheral edema, ascites and pleural effusion. These clinical
signs reflect the hypoalbuminemic patient's impaired ability to hold fluid within the vascular space, and usually only occur
when plasma albumin levels drop to between 10 and 16 g/L. The fluid that typically leaks into extravascular spaces is a pure
transudate:
Pure Transudate:
Clear and colorless
Protein < 25 g/L
Specific Gravity < 1.018
Few cells (if any) seen
Decreased oncotic pressure and loss of intravascular fluid can also lead to hypovolemia, which in turn can lead to problems
such as poor peripheral perfusion and pre-renal azotemia.
Causes of Hypoalbuminemia
The potential causes of hypoalbuminemia are many, and include:
Hepatic failure (failure of albumin synthesis)
Gastrointestinal protein loss (protein-losing enteropathies)
Renal protein loss (protein-losing nephropathies)
Other external losses in exudate or hemorrhage
Hyperglobulinemia (with a 'compensatory' decrease in albumin production)
Starvation/protein malnutrition
Chronic illness
Hypoadrenocorticism
Laboratory error
Despite this multitude of potential etiologies, the diagnostic approach to hypoalbuminemia is usually very straightforward.
Non-gastrointestinal and non-renal causes of external protein loss (such as third degree burns, open pyometra, and draining
pyothorax or peritonitis) are usually obvious, while hyperglobulinemia, starvation, protein malnutrition and chronic illness
rarely cause more than mild hypoalbuminemia. With the possible uncommon exception of hypoadrenocorticism, moderate to severe
hypoalbuminemia can therefore usually be narrowed down to only three major potential causes:
1. Hepatic failure
2. Protein-losing enteropathy
3. Protein-losing nephropathy
