Haemostatic changes in systemic inflammatory response syndrome during continuous renal replacement therapy

BACKGROUND
Endothelial damage and hemostatic imbalance play an important role in the evolution of the Systemic Inflammatory Response Syndrome (SIRS) into the Multiple Organ Dysfunction Syndrome (MODS). In Acute Renal Failure associated with SIRS, different types of Continuous Renal Replacement Therapies (CRRT) may give non-renal benefits by modifying the levels of some factors related to those disturbances.

METHODS
Forty patients with SIRS-associated ARF were randomised to receive either continuous venovenous hemofiltration (CVVH) or continuous venovenous hemodiafiltration (CVVHDF) for the first 24 h. Afterwards the CRRT method was reversed. The group treated with CVVH moved to CVVHDF and that treated with CVVHDF to CVVH for the next 24 h. Plasma levels of: von Willebrand Factor (vWF), thrombomodulin, plasminogen activity inhibitor type 1 (PAI-1: antigen and activity), tissue type plasminogen activator (t-PA: antigen), prothrombin fragment 1+2 (F1+2) and thrombin-antithrombin complexes (TAT) were measured previously to CRRT (base-line), and after 24 and 48 hours of therapy. Multivariate ANOVA was the statistical method used.

RESULTS
In the MANOVA study a significant decrease in PAI-1 activity during the treatment procedure was observed (horizontality p <0.05). PAI-1 antigen showed a tendency to decrease although without statististical significance. There were no significantly different changes in the other factors analysed during either CRRT (parallelism p >0.05). At the base-line point, all the factors were higher than normal values in healthy adults.

CONCLUSIONS
The present study suggests that CRRT, in patients with SIRS, may promote a decrease in PAI-1 and consequently, a better outcome. There were no differences between the CVVH and the CVVHDF methods regarding the factors analysed. The present data confirms that there is an important endothelial and hemostatic dysfunction in SIRS from the early phases.

CITATION   J Nephrol. 2000 Jul-Aug;13(4):282-9