To evaluate a possible interaction between coagulation factors, inflammation, and immunological disorders in the pathogenesis of glomerulonephritis (G.N.) factor VIII clotting activity (VIII:C), related-antigen (VIIIR:AG), urinary fibrinogen degradation products (F.D.P.) excretion and cyclic nucleotides (cAMP) in 21 patients affected by chronic G.N. with normal renal function, was investigated. These patients were followed-up for two years. For the assay of factor VIII:C, a factor VIII deficient plasma was used. Factor VIIIR:AG were assayed by rocket electroimmunodiffusion in agarose gel, urinary F.D.P. by Thrombo-Wellcotest and cAMP by radioimmunoassay. The same tests were performed in 25 healthy controls. Patients' clotting activity, measured at first admission, showed a significant decrease in comparison with the values obtained at the end of the follow-up period (t=-2.61 p<0.02).The clotting activity of the renal patients was lower than in controls (t=2.09 p<0.05). However, factor VIIIR:AG was significantly increased in the same patients. A significant direct correlation between the urinary excretion of cAMP and plasma concentration of factor VIIIR:AG (r=0.82 p<0.001) as well as between urinary F.D.P. and cAMP excretion (r=0.49 p<0.05) was found, when the patients were classified according to the morphological findings of the kidney biopsy. Most probably a circulating thrombin excess leads to consumption of factor VIII:C and promotes the extrusion of cyclic nucleotides from intracellular sites. The relationship found between factor VIIIR:AG, cAMP and F.D.P. besides showing a linkage between inflammation and coagulation, seems also to suggest a role for both factors in promoting a renal injury.
Stimulation of fibrinogen synthesis: a possible functional role of fibrinogen degradation products
