Factor VIII Procoagulant Activity in Children with Nephrotic Syndrome and Post-Streptococcal Glomerulonephritis

Adhikari, M.; Coovadia, Hoosen; Greig, H. B. W.; Christensen, Søren

doi:10.1159/000181466

Cited by 13 publications

(4 citation statements)

References 9 publications

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“…In addition, disturbances of liver protein syn theses are present in NS and seem dependent, at least partly, on hypoalbuminemia. While synthesis of albumin may be normal or only slightly increased [33,34], that of fibrinogen and transferrin is markedly increased [14,35], In nephrotic rats with Heymann nephritis, immunocytochemical methods disclosed an increased number of hepatocytes containing fibrinogen [36], suggesting that enhanced liver synthesis, in the absence of urinary loss, accounted for hyperfibrinogenemia; in contrast there were no changes in the number of cells containing albu min or AT III, and therefore no compensation for uri nary loss of both proteins [36], Most studies in humans are in agreement with these results and have shown cor relations between the intensity of coagulation disorders and the intensity of albuminuria and hypoalbuminemia [1,4,5,7,8,15,23], as already mentioned for AT III disorders.…”

Section: Abnormalities Of Coagulation and Fibrinolysis Factors In Sysmentioning

confidence: 89%

Coagulation Factors in Nephrotic Syndrome

Kanfer¹

1990

Am J Nephrol

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Nephrotic syndrome (NS) is associated with several disorders of hemostasis: thrombocytosis and platelet hyperaggregability; increased plasma levels of factors V and VIII, and of fibrinogen with blood hyperviscosity; decreased plasma levels of natural anticoagulants: free protein S, and antithrombin III compensated by increased levels of α₂-macroglobulin; lowered fibrinolytic activity. Intensity of hypercoagulability is related to the degree of hypoalbuminemia; however, the role of hypercoagulability in the increased incidence of thromboembolic events, including renal vein thrombosis, is not proved. Clotting disorders are due to urinary losses of anticoagulants or to increased liver synthesis of procoagulants stimulated by hypoalbuminemia. Moreover, changes in clotting factors levels may be due to intravascular thrombin formation (marked by increased plasma levels of fibrinopeptide A). During active phases of glomerulonephritides (GN) with NS, thrombin formation might in fact arise in glomeruli, following activation of the glomerular hemostasis system. Isolated glomeruli from human crescentic GN, rabbit nephrotoxic GN and rat HgCl₂ autoimmune GN produce excessive amounts of procoagulant (tissue factor) activity (PCA). Sequential studies of the self-limited HgCl₂ GN showed that glomerular PCA, proteinuria and glomerular fibrin deposits peaked concomitantly at the acme of the disease, suggesting that immunologically mediated glomerular damage had triggered the extrinsic coagulation pathway.

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Section: Abnormalities Of Coagulation and Fibrinolysis Factors In Sysmentioning

confidence: 89%

Coagulation Factors in Nephrotic Syndrome

Kanfer¹

1990

Am J Nephrol

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“…Of several series screening hemostatic protein abnormalities in nephrotic syndrome patients, Kanfer et al (9) described elevated levels of factors V, VIII and fibrinogen and thrombocytosis. High factor VIII activities may be prognostically useful in some patients urith renal diseases (35) and are accompanied, as in the present series, by elevations of factor Vlll-related antigen (von Willebrand factor) (36,37). Except for one case (38), increased clotting activities of factors VII and X have also been noted in nephrotic slmdrome patients (11).,Although high levels of these factors are often associated with "h54tercoagulable" states, a lack of correlation with thrombosis is noteworthy; as in other clinical situations, elevations presumably reflect changes associated with inflammation.…”

Section: Discussionmentioning

confidence: 99%

Factor XII and Other Hemostatic Protein Abnormalities in Nephrotic Syndrome Patients

Thompson

1982

Thromb Haemost

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SummaryFactor XII clotting activities and antigen levels were assayed in 14 plasma samples from 10 patients with nephrotic syndrome; the group was heterogeneous clinically and histologically. Factor XII was low at initial sampling in 7 of the 10 patients; in 7 of the 14 samples, factor XII antigen was in excess over clotting activity. Inhibition of factor XII could not be demonstrated; excess plasma antigen and urinary antigen (when present) had normal patterns on crossed-immunoelectrophoresis, indicating no major changes in charge or size. In 3 patients tested more than once, plasma levels of factor XII were increased up to 6fold in steroid-induced remission.Of other hemostatic factors assessed for comparison, factor VIII was elevated in 11 of the 14 samples; eight of these had elevated factor VII levels as well. Eight samples from six patients showed low antithrombin III levels; one of these patients had recurrent thromboses. Antithrombin III levels correlated with the serum albumin concentration.Only two of the eight urines tested had detectable factor XII antigen; a third had factor IX and prothrombin and no factor XII. Plasminogen and antithrombin III were readily demonstrated in all urine samples with higher concentrations in those patients with less selective proteinuria. Urinary and plasma levels were not correlated, suggesting that increased consumption or turnover was not simply related to increased filtration.

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“…Hemorheology is altered by multiple triggers such as blood hypercoagulability, hyper viscosity, platelet hyperaggregability, a defective deformability of red blood cells, hyperaggregation of red blood cells in the presence of low fluid shear stress or hypoperfu sion, an increase in blood elements, and vessel wall inter action due to the increased expression of adhesion mole cules. Therefore, a progressive reduction in blood and its ischemic consequences are due to a deficiency in both the quality and quantity of blood [69,70,[90][91][92][93][94][95][96][97],…”

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confidence: 99%

Glomerular Endothelial Dysfunction Determines Disease Progression: A Hypothesis

Futrakul¹,

Sitprija²,

Yenrudi³

et al. 1997

Am J Nephrol

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A glomerular endothelial funciton with its hemodynamic impact is proposed to determine disease progression. In the clinical settings associated with an intact endothelial function, such as minimal-change steroid-sensitive nephrosis, the early phase of diabetes mellitus and the early stage of an experimental model of renal ablation in animals, it was observed that adequate renal perfusion correlates with the intact structure and function of the nephron with no evidence of disease progression. In contrast, the clinical settings associated with endothelial dysfunction, such as chronic glomerulonephropathy, the late stage of diabetes mellitus and a renal ablation model in animals, are usually associated with a reduction in renal perfusion. The magnitude of renal hypoperfusion observed in all forms of chronic glomerulonephropathies is proportional to the degree of clinical severity. A progressive pattern of renal hypoperfusion is uniquely observed when disease severity progresses. In this context, a new therapeutic maneuver aiming to improve renal perfusion is proposed for treating glomerulonephropathy with disease progression and preventing it from developing to end-stage renal disease.

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Factor VIII Procoagulant Activity in Children with Nephrotic Syndrome and Post-Streptococcal Glomerulonephritis

Cited by 13 publications

References 9 publications

Coagulation Factors in Nephrotic Syndrome

Coagulation Factors in Nephrotic Syndrome

Factor XII and Other Hemostatic Protein Abnormalities in Nephrotic Syndrome Patients

Glomerular Endothelial Dysfunction Determines Disease Progression: A Hypothesis

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