Hypercoagulation in glomerulonephritis

The clotting values of 50 patients with glomerulonephritis were examined. Three different coagulation groups were recognised: those with normal clotting values (group 1); those with high concentrations of factor VIII but otherwise normal clotting results (group 2); and patients who showed the presence of an activator of the intrinsic coagulation pathway, indicated by the presence of a short activated partial thromboplastin time or the ability of patients' plasma to shorten control clotting time in mixing studies (group 3). Patients in group 2 either had a uniform rise in all three components of the factor VIII molecule or a disproportionately higher concentration of factor-VIII-related antigen. In contrast, the level of VIII clotting activity in patients in group 3 was always higher than concentrations of either VIIIAg or VIIIWF. A significantly high incidence of thrombotic complications was observed in patients in group 3 but in none of the patients in either group 1 or group 2. Impaired renal function was more common in patients in groups 2 and 3, with higher mean serum creatinine concentrations in those in group 3. Patients with glomerulonephritis who have a short partial thromboplastin time with kaolin or who shorten control clotting time form a subgroup in whom hypercoagulation could adversely affect the course of their disease. The value of antiplatelet or anticoagulant treatment in these patients needs to be explored. Monash University Department of Medicine, Alfred Hospital, Prahran, Victoria 3181, Australia HATEM H SALEM, MRCP, lecturer JERRY KOUTTS, FRACP, senior lecturer BARRY G FIRKIN, FRACP, professor Department of Nephrology, Royal Melbourne Hospital, Parkville, Victoria 3050, Australia JUDITH A WHITWORTH, FRACP, senior lecturer in medicine PRISCILLA S KINCAID-SMITH, FRACP, professor of medicine Introduction The role of the coagulation process in the pathogenesis of glomerulonephritis and its complications have become increasingly recognised. Experimental evidence aInd findings on pathological examination of kidneys from patients with glomerulonephritis suggest that local intravascular coagulation plays an important role in the progression of the renal disease.' In these patients the presence of a systemic hypercoagulable state may contribute to the deterioration of renal function and may be associated with a high incidence of thrombotic complications. In patients with established nephrotic syndrome a high incidence of thromboembolic phenomena has been reported.2 The observed high concentrations of factors V and VIII3 and low concentrations of antithrombin III4 are thought to be important in the pathogenesis of this complication. The clotting values of other patients with glomerulonephritis have, however, received little attention in recent reports. This paper reports an investigation of the clotting values of 50 patients with glomerulonephritis and establishes the incidence of a coagulation accelerating factor recognisable in vitro and its possible influence on the clinical course of these patients. Patients and methods Fifty patients (24 men, 26 women) aged from 12 to 78 years (mean 37±16) were examined. In all patients the diagnosis of glomerulonephritis was confirmed by renal biopsy. Two additional groups served as controls: (a) 20 healthy individuals (medical and laboratory personnel), and (b) 70 ageand sex-matched inpatients with various medical disorders. These inpatients included 20 patients with renal disease not characterised by glomerulonephritis but with a comparable degree of renal impairment as the study group and 50 with various disorders such as ischaemic heart disease, cerebrovascular accidents, chronic bronchitis, collagen disease, malignant lymphoma, and thyroid disease. None of the control patients were known to have a haemorrhagic tendency. Blood was collected in 1/10 volume 3 8% trisodium citrate. Plateletpoor plasma was obtained by centrifugation at 2000 g for 15 minutes. Prothrombin, thrombin, and Stypven times were measured by standard methods. Partial thromboplastin time with kaolin (PTTK) was measured by incubating 0-1 ml of plasma with 0-05 ml kaolin 50 mg/ml and 0-05 ml Platelin (General Diagnostics) for 3 minutes on 13 N ovem er 2019 by gest. P rocted by coright. hp://w w w bm jcom / B r M ed J (C lin R es E ): frst pulished as 10136/bm j.28282.2083 on 27 Jne 181. D ow nladed fom