Serum levels of fibrin-fibrinogen degradation products in the haemolytic-uraemic syndrome.

Uttley, W. S.

doi:10.1136/adc.45.242.587

Cited by 10 publications

(6 citation statements)

References 7 publications

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“…In addition, these patients showed increased fibrinolytic turnover, as measured by D-dimer levels, with increased plasma t-PA and PAI antigen levels, and an overall decrease in plasma fibrinolytic potential due to a net increase in PAI-1 activity. The increased levels of PAI-1 activity and t-PA are supported by the results of previous studies [161,164,165]. High levels of D-dimer can result from the local fibrinolysis, even if the plasma fibrinolytic activity is decreased [165].…”

Section: Fibrinolysis and Coagulationsupporting

confidence: 74%

Pathogenesis of Shiga toxin-induced hemolytic uremic syndrome

Ray

2001

Pediatric Nephrology

144

146

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Section: Fibrinolysis and Coagulationsupporting

confidence: 74%

Pathogenesis of Shiga toxin-induced hemolytic uremic syndrome

Ray

2001

Pediatric Nephrology

144

146

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“…On the basis of these results, it was thought that there is no activation of coagulation in childhood HUS (6). However, increased levels of fibrin degradation products in urine (9) and plasma (5,10), and raised levels of fibrinopeptide A (1 1) suggest otherwise. More sensitive markers of activation of coagulation such as thrombin-antitluombin III (TAT) and prothrombin fragment l+2 (F1+2) are now available.…”

Section: Lntroductionmentioning

confidence: 97%

Activation of Coagulation and Fibrinolysis in Childhood Diarrhoea-associated Haemolytic Uraemic Syndrome

et al. 1997

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SummaryDiarrhoea-associated haemolytic uraemic syndrome (D+ HUS) is usually caused by verotoxin producing Eschericia coli. We hypothesized that verotoxin binding to glomerular endothelial cells causes localised endothelial cell activation and thus activation of coagulation and reduction of fibrinolytic potential. We also proposed that treatment with fresh frozen plasma or dialysis would not affect these changes. Markers of activation of coagulation and fibrinolysis were measured in 30 children with acute D+ HUS serially, in healthy children and in children on dialysis.In acute D+ HUS, levels of thrombin-antithrombin III complex and prothrombin fragment 1+2 were significantly increased (p <0.001). The source of thrombin generation was unclear. Factor Xlla levels were increased in patients and controls with renal failure. Factor VIIa levels were not significantly raised in children with acute D+ HUS. D-dimers were increased, but fibrinolytic potential as measured by fibrin plate was reduced. Levels of plasminogen activator inhibitor antigen and activity and tissue plasminogen activator antigen were increased.Neither peritoneal dialysis nor administration of blood products, the most common treatments, altered parameters of coagulation or fibrinolysis.

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“…The most recent publications offer clear evidence that intravascular coagulation is a fundamental intermediary mechanism of the HUS [5,8,17,42,48,53]. 56 patients were studied by our group with serial evaluations of the clotting mechanisms.…”

Section: Coagulation Studiesmentioning

confidence: 99%

The Hemolytic-Uremic Syndrome

Ca¹,

Vitacco²,

Mendilaharzu³

et al. 1973

Nephron

249

132

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The clinical and pathological characteristics of the acute stage of the HUS are described on the basis of 678 patients and the study of 52 autopsies and 3 kidney biopsies. The laboratory and pathological studies point to DIC as a basic pathogenic mechanism, probably related to a viral infection. The recent mortality rate has been 6.25% due to the exacting dialysis treatment employed. Heparin was ineffective in the 26 patients in which it was used. 124 patients have a follow-up of more than 5 years and up to 13 years. 60 patients are completely recovered, while 64 have persistent signs of renal disease. Nine other children died in uremia 1–12 years after onset. The pathological findings are discussed on the basis of 6 autopsies and 24 biopsies in 27 patients. This stage of the HUS appears as an important and new aspect of pediatric nephrology.

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Serum levels of fibrin-fibrinogen degradation products in the haemolytic-uraemic syndrome.

Cited by 10 publications

References 7 publications

Pathogenesis of Shiga toxin-induced hemolytic uremic syndrome

Pathogenesis of Shiga toxin-induced hemolytic uremic syndrome

Activation of Coagulation and Fibrinolysis in Childhood Diarrhoea-associated Haemolytic Uraemic Syndrome

The Hemolytic-Uremic Syndrome

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