Erythrocyte aggregation and sedimentation is determined by the concentration of high molecular plasma proteins such as fibrinogen and immunoglobulins. The role of albumin, the most abundant plasma protein, is controversial. We analysed the influence of human albumin (0-80 g L-1) on sedimentation behaviour of erythrocytes suspended (haematocrit 35%) in fibrinogen-enriched normal plasma, plasma from patients with hypoalbuminaemia, solutions of dextran 70 in buffer, and mixtures of fibrinogen, immunoglobulins and albumin in buffer. Sedimentation was measured by the Westergren method, viscometry was performed at low and high shear rate. The addition of albumin to normal plasma, hypoalbuminaemic plasma, or dextran solutions in buffer decreased the erythrocyte sedimentation rate. In contrast, in a mixture of fibrinogen and immunoglobulins in buffer, albumin increased erythrocyte sedimentation. When either fibrinogen or immunoglobulins were omitted, or fibrinogen was replaced by dextran, albumin did not increase sedimentation, which indicates that increased sedimentation was due to an interaction of all three compounds. The viscosity of erythrocyte suspensions was increased by albumin. It is concluded that the influence of albumin on erythrocyte aggregation is complex and depends on the technique used; low shear viscosity is increased, but erythrocyte sedimentation, i.e. under no flow conditions, is decreased. The inhibitory action of albumin on the erythrocyte sedimentation rate has clinical implications and must be known by physicians. It may help to interpret sedimentation rates more correctly and prevent misinterpreting presumed therapeutic successes or failures.