Effect of increasing serum albumin on haemostatic factors synthesized in the liver in CAPD patients.

BACKGROUND

This study was performed to evaluate the relationship between serum albumin and plasma concentration of haemostatic factors and the effect of raising serum albumin on haemostatic factors synthesized in the liver in CAPD patients.

METHODS

We measured blood levels of albumin, fibrinogen, factor II, factor VII, protein C, free protein S, plasminogen, alpha2-antiplasmin and antithrombin III in 103 CAPD patients and 30 normal controls. Twenty-two patients with albumin < 3.5 g/dl were divided into two groups. In the experimental group (n = 11), haemostatic factors and albumin were measured before, after repeated infusion of 20% albumin 100 ml three times per week for 2 weeks, and 4 weeks after withdrawal of albumin infusion. The same parameters were measured in the control group (n = 11) which did not receive albumin infusion. C-reactive protein and haematocrit were followed in both groups as an indicator of acute phase reactant and an indirect measure of volume status.

RESULTS

CAPD patients as a whole had lower albumin and higher fibrinogen and factor VII than normal controls. A significant inverse correlation was present between fibrinogen and albumin (r = -0.27, P < 0.01). Albumin in the experimental group increased from 2.7 +/- 0.4 to 3.5 +/- 0.6 g/l at the end of its repeated infusion and haematocrit decreased from 26.6 +/- 4.4 to 24.9 +/- 5.2%. Fibrinogen and factor VII decreased significantly, even after correction for haematocrit (624 +/- 96 vs 556 +/- 91 mg/dl, 160 +/- 36 vs 121 +/- 44%, P < 0.05). Four weeks after withdrawal of albumin infusion, serum albumin decreased to 2.7 +/- 0.5 g/dl, whereas fibrinogen and factor VII increased to 619 +/- 78 mg/dl and 158 +/- 32%, respectively (P < 0.05). Albumin, haematocrit and haemostatic factors in the control group did not change. CRP was stable during the study period in both groups.

CONCLUSION

These findings indicate that hypoalbuminaemia is an important trigger factor in the elevation of fibrinogen, and possibly factor VII, in CAPD patients.