In the spirit of #DietitiansWeek & #MythbustingMonday, I thought I would chip in with one that has been a staple throughout my clinical training: Albumin is not a good marker of nutritional status. Below is a thread of some simple things I have learned (1/10)
I remember this being said in an early biochemistry lecture and it always stuck with me - for a long time without ever really understanding why (2/10)
What causes low albumin? Very often this is a result of an inflammatory state. We often observe rising inflammatory markers (CRP) coinciding with low albumin status. This much seems to be widely understood - but why? (3/10)
Inflammation contributes by
1. Increasing capillary permeability (this gives albumin a chance to move out of cells, in normal circumstances it is too big to do so)
2. Reducing half-life of albumin (this means it doesn’t stay around as long as usual) The result? Low albumin (4/10)
Because albumin is a primary contributor to plasma oncotic pressure (holding water in cells), when it is released it means that water goes with it. This result = Oedema (fluid overload) (5/10)
Because albumin is a protein, there is a misconception that a ‘high protein diet’ can correct this. This tends to be a frequent topic of conversation between dietitians and doctors on the wards (6/10)
The case for albumin = nutritional status. It's complicated
- In many undernourished patients, in the absence of inflammation, albumin remains normal (Anorexia patients)
- In well nourished patients, the presence of inflammation can result in low albumin (pregnant women) (7/10)
So what is the main message here and what do you say if you receive a referral for ‘low-albumin’:
- The target of treatment should really be the route of the existing inflammation
- This means that nutrition support will not ‘fix’ the issue of low albumin (8/10)
BUT: 
Low albumin and malnutrition often co-exist, and many patients with low albumin require and will benefit from nutrition support (9/10)
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