Specimen Collection

Sample stability :

• 2.5 months at 15-25 ^o C
• 5 months at 2-8 ^o C
• 4 months at -20 ^o C

4.5 mL PST Blood (Preferred)

0.5 mL Paediatric Micro-PST Blood (Preferred)

5 mL Heparin Blood

4 mL Plain Blood

3.5 mL SST Blood

0.5 mL Microsample Blood

0.5 mL Paediatric Micro-heparin Blood
Reference Intervals

Units : g/L

Age
0 - 3 months	25 - 40
3 - 12 months	32 - 45
> 1 year	32 - 48

Pregnancy
2 - 14 weeks	32 - 45
14 - 28 weeks	27 - 37
28 - 42 weeks	25 - 35

Uncertainty of Measurement: 6%

Download: New albumin method: detailed information - Albumin method change document - August 2014.docx

Turnaround Time: Within 3 hours
Assay Method

Principle : Dye-binding to bromocresol purple (BCP)

Analyser : Cobas

Diagnostic Use and Interpretation

Increased albumin concentrations are either due to prolonged venostasis during specimen collection (artefactual), or dehydration.

Decreased concentrations may be due to

• dilution (IV fluids, specimen taken from "drip arm"),
• decreased synthesis ( liver failure)
• increased loss (nephrotic syndrome, burns, protein-losing enteropathy)
• shift to extravascular space (inflammation, trauma)
• increased catabolism ( malignancies, thyrotoxicosis, inflammation).
• analbuminemia (a rare genetic disorder)

Serum albumin is NOT a nutritional marker

Serum albumin decreases in response to a wide range of illnesses and trauma. Inflammation causes a cytokine-mediated shift to the extravascular space. Conversely, even severe malnutrition states such as marasmus and anorexia nervosa are not usually accompanied by decreased albumin levels. The only malnutrition state associated consistently with low albumin is Kwashiorkor. For these reasons, albumin is not useful as a nutritional marker, despite its traditional use in this role.

Serum-Ascites Albumin gradient (SAAG):

SAAG i.e. Plasma albumin minus by Ascitic fluid albumin (in g/L) has been used to distinguish 2 big groups of causes for ascites :

- portal hypertension related (e.g. liver cirrhosis or congestive heart failure) with SAAG described in literature as usually >=11g/L

- non-portal hypertension related (e.g malignant ascites, tuberculosis, pancreatitis) with SAAG described in literature as usually <11g/L

However, using cut point of 15g/L instead of 11g/L may improve sensitivity for non-portal hypertension related causes without losing specificity.

References

1. Lee JL et al. (2015): Serum albumin and prealbumin in carorically restricted, nondiseased individuals: a systematic review. Am J Med 128:1023.e1-1023.e22

2. Friedman, A. N. and S. Z. Fadem (2010). "Reassessment of albumin as a nutritional marker in kidney disease." J Am Soc Nephrol 21 (2): 223-230.

Contact Information

Emails to chemicalpathologist@adhb.govt.nz will receive priority attention from the on-call chemical pathologist.

If the query concerns a specific patient please include the NHI number in your email.

If email is not a suitable option, please contact the on-call chemical pathologist via Lablink (Auckland City Hospital ext. 22000 or 09-3078995).

Individual chemical pathologists may be contacted but will not be available at all times.

After-hours : contact Lablink (Auckland City Hospital ext. 22000 or 09-3078995) or hospital operator for on duty staff after hours.

Dr Samarina Musaad (Clinical Lead) : SamarinaM@adhb.govt.nz ext. 22402

Dr Cam Kyle: CampbellK@adhb.govt.nz ext 22052

Dr Weldon Chiu: WeldonC@adhb.govt.nz ext. 23427

Dr Campbell Heron: CHeron@adhb.govt.nz ext. 23427

Dr Sakunthala Jayasinghe: Sakunthala@adhb.govt.nz ext. 23427