Introduction:
Fetuin (AHSG, or Fetuin-A) has the highest capacity in inhibiting soft tissue calcification among all other
molecules in the circulation. It is the most important and major calcification regulating protein in the
circulation.
Fetuin, a glycoprotein present in the circulation, is synthesized by hepatocytes. The fetuin molecule
consists of two polypeptide chains, which are both cleaved from a proprotein encoded from a single
mRNA. The protein is commonly present in the cortical plate of the immature cerebral cortex and bone
marrow hemopoietic matrix. However, its function of inhibiting soft tissue calcification is achieved by
forming a soluble colloidal microsphere of fetuin-calcium-phosphate complex in the blood stream.

Clinical Applications:
For patients with uremia on dialysis, a higher Ca x P product level accomplished with an abnormally lower fetuin
level would have an extremely high risk of ectopic tissue / cardiovascular calcification. Even for those patients
with an acceptable Ca x P product level, but an abnormal fetuin level the risk of calcification would be increased
(please read the references below for more details)

• Risk assessment of ectopic tissue calcification in chronic renal failure
• Monitoring of soft tissue calcification in renal transplant recipients
• Calciphylaxes
• Diabetes related vascular calcification
• Risk stratification of acute coronary syndromes
• Arteriosclerosis related research
• Heart, aorta, valves calcifications

Human Fetuin ELISA:

Assay format: “sandwich” immunoenzymometric assay using two polyclonal human fetuin specific antibodies
Patient sample: serum
Sample volume required: 0.1 mL
Normal range: 0.4 – 0.95 g/L
Assay incubations: < 2 hours

References:

• Schafer C, et al. The serum protein alpha 2-Heremans-Schmid glycoprotein/fetuin-A is a systematically acting inhibitor of ectopic calcification. J Clin Invest. 2003 Aug 112(3):357-66
• Ketteler M, et al. Association of low fetuin-A (AHSG) concentrations in serum with cardiovascular mortality in patients on dialysis: cross-sectional study. Lancet. 2003 Mar 8;361(9360):827-33
• Ketteler M, et al. Deficiencies of calcium-regulatory proteins in dialysis patients: a novel concept of cardiovascular calcification in uremia. Kidney Int Suppl. 2003 May; (84):S84-7. review.