In vivo measurements of fibrin formation and degradation in nephrotic patients |
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Authors: | Andrea Sagripanti Adamasco Cupisti Ugo Baicchi Marco Ferdeghini Giuliano Barsotti |
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Institution: | (1) Ist Clinical Medicine Institute, University Hospital, Via Roma 67, 1-56126 Pisa, Italy;(2) Blood Bank, University Hospital, Via Roma 67, I-56126 Pisa, Italy;(3) Nuclear Medicine Service, University Hospital, Via Roma 67, I-56126 Pisa, Italy;(4) Clinical Medica I, Ospedale S. Chiara, I-56126 Pisa, Italia |
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Abstract: | Summary Intraglomerular fibrin deposition has been implicated as an important pathogenetic mechanism in patients with glomerular diseases
and the nephrotic syndrome. To investigate fibrin formation and degradation in nephrosis, we measured fibrinopeptide A by
radio-immunoassay and D-dimer by enzyme-linked immunosorbent assay in the plasma of 30 consecutive adult patients with the
nephrotic syndrome; in 10 the serum creatinine was more than 2 mg/dl. Both fibrinopeptide A and D-dimer were abnormally elevated
in the majority of nephrotics (P<0.001 vs. healthy controls), providing evidence of increased fibrin generation and lysis “in vivo.” A positive correlation
was found between fibrinopeptide A and D-dimer (correlation coefficient 0.64,P<0.001), suggesting a close relationship between fibrin formation and degradation. Calcium heparin, administered to 12 nephrotics,
caused a marked decrease in plasma fibrinopeptide A, due to a reduction of in vivo thrombin activity. As enhanced thrombin
activity can favor fibrin deposition within the renal parenchyma, as well as vascular complications, it is reasonable to assume
that an antithrombotic treatment aimed at controlling thrombin generation may ameliorate the natural history of nephrosis. |
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Keywords: | Nephrotic syndrome Fibrinopeptide A D-dimer Fibrin Calcium heparin |
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