Albumin Binding Capacity (ABC) - a new approach for assessment of albumin transport function and its potential clinical use

Reduction of serum albumin concentration is correlated with an increased mortality in different diseases, therefore albumin concentration is seen and used as an independent predictor of severity of illness in different clinical scoring systems. However, estimation of albumin concentration does not provide information about the existing functional status or capacity to transport endogenous substances (e. g. prostaglandins, bilirubin, bile acids, fatty acids, thyroid hormones, endogenous steroids and benzodiazepines) or drugs (e. g. diuretics, ß-Lactam-antibiotics, sedatives).

Especially in acute liver failure or in end stage liver disease (ESLD) the impaired excretory capacity for lipophilic substances leads to an accumulation of these mostly albumin bound or transported compounds. According to the reduced albumin concentration and the limited transport capacity substances with a less affinity will be competitive displaced by ligands with a higher binding affinity to albumin. Metabolic pathways can be affected by the so increased unbound fraction of various substances which can results in worsening of hepatic failure or impaired pharmacokinetic or toxic effects of drugs.

Considering the need of a simply estimation of existing albumin transport function especially in liver disease a new laboratory test has been developed which enables the binding site specific characterization of the Albumin Binding Capacity (ABC). Measuring either the bound (direct test) or the unbound (indirect test) fraction of a site specific marker and comparison with a reference the available transport capacity can be expressed quantitatively.

In in-vitro experiments the expected decrease of ABC with increasing levels of thyptophan or benzodiazepines could be confirmed, as well as a reduced ABC in commercially available albumin preparations with a high amount of albumin bound stabilizers like N-Acetyl-Tryptophan or Caprylate.

In first clinical evaluations a significant reduction in ABC for patients with a severe deterioration of ESLD and excretory liver failure could be shown, whereas in a group of healthy volunteers the ABC was comparable to Fresh Frozen Plasma as well as to albumin preparations without stabilizers.

During clinical MARS treatments the reduced ABC could be improved, consistent with the elimination of albumin bound substances and the correction of albumin overload in this therapeutic procedure.

With the characterization of albumin transport capacity this new laboratory test offers the opportunity to take into consideration not only the amount but also the function of albumin as predictive prognostic value in liver disease and as a possible helpful tool to support decisions for therapeutic procedures like albumin substitution or MARS treatments. This assumed potential of the ABS test has to be confirmed by ongoing clinical trials.