Most chronic liver diseases are notoriously asymptomatic, until cirrhosis with clinical decompensation occurs. The use of early diagnosis strategies is vital to maintain patients in a symptom-free state and to delay decompensation, and thus improve the outcome. Albumin (HAS) undergoes several post-translational modifications in hepatocytes but clinical relevance of some of these modifications has been recently investigated in advanced liver diseases. Now, the inventors demonstrate that the binding capacities of some ligands, measured by inductively coupled plasma mass spectrometry (ICP-MS), are significantly different between cirrhotic patients and patients with no liver dysfunctions. The decreased binding capacities in cirrhotic patients were paralleled by the presence of significantly higher HSA isoforms. Animal experimentations were also conducted to explore the precocity of HSA modifications in the course of chronic liver dysfunction. This allow the inventors to assume that the most important modifications of albumin structure due to liver dysfunction could be revealed by measuring the unbound fraction of specific ligands spiked in serum.