Clotting Abnormalities During The Course Of Immune Type Glomerulonephritis Induced By HgCl₂ In The Brown Norway(BN) Rat

This work was undertaken in order to study the clotting process during the course of a biphasic immune type glomerulonephritis(GN) induced by HgCl₂ in the Brown Norway (BN) rat. This toxic agent induced, in a first stage, the formation of antiglomerular basement membrane (GBM) antibodies and in a second stage an immune complex type GN.

Antithrombin III (AT III), fibrinogen degradation products (FDP) were evaluated by electroimmunodiffusion using specific antisera. The other classical methods were performed using commercial reagents. The albumin platelet content was evaluated by a radioimmunoassay. The soluble fibrin monomer complexes (FM) were searched for by a chromatographic technic.

Transient clotting proteins variations related to nephrotic syndrome were observed (low AT III level, low factor XII activity, increased factor V activity, and increased fibrinogen level). Disseminated intravascular coagulation (DIC) was suggested by low platelet counts, rise in FDP, and presence of FM. Fibrin thrombi in the glomerular capillaries were observed by immunofluorescence in the rats presenting evidence for DIC and in rats which died during the first phase of the disease. The animals presenting DIC syndrome were the most severy ill.

The hypothesis of an activation of the haemostasis system was supported by a low albumin platelet content and by the existence of high molecular weight fibrinogen derivatives. Complement activation, immune complexes, endothelial lesion might trigger DIC : the mechanism responsable for initiation of DIC are under study.

According to this results, it can be concluded that DIC which is responsable for the death of several animals, plays a major pathogenic role in this experimental autoimmune disease.