INTRAVASCULAR COAGULATION IN ACUTE GLOMERULONEPHRITIS (AGN)

Abstract

Evidence exists that intrarenal intravascular coagulation occurs in certain renal diseases, but its role in the genesis of chronic renal disease remains controversial. Plasma chromatography (Fletcher et al., Trans. Amer. Assoc. Phys., 1970) was performed serially in 51 children with post-streptococcal AGN. This method quantifies the relative proportions of fibrinogen complexes, monomeric fibrinogen and fibrinogen derivatives smaller than fibrinogen in plasma. Intravascular coagulation/thrombosis is characterized by increase in fibrinogen complexes and fibrinolysis by increase in smaller fibrinogen derivatives. In the acute phase of AGN, the mean level of fibrinogen complexes was 19.2% (control 57., p < .001). With diuresis, complexes fell to 12.2% (days 1-5) and 9.3% (days 6-10). Fibrinogen breakdown products were elevated in the acute and early diuretic phase, but significantly so only at 6 days and later (6-10 days, 35.8% vs. 23% control, p < .01). Pathological complex concentrations were found in those with the more severe disease. In the acute phase, factor XIII and α2-macroglobulin were significantly reduced, antithrombin III was reduced but not significantly (mean 92% of control). Fibrinogen was raised in the acute phase, but only became significantly so in the early recovery phase (369 mg% vs. control 292 mg%, p < .01). After recovery from AGN, all parameters returned to control values. The study indicates that intravascular fibrin deposition, presumably intraglomerular, occurs during the acute stage of AGN, but resolves during recovery.