IN-VIVO MEASUREMENTS OF FIBRIN FORMATION AND DEGRADATION IN NEPHROTICPATIENTS

Intraglomerular fibrin deposition has been implicated as an important pathogenetic mechanism in patients with glomerular diseases and the ne phrotic syndrome. To investigate fibrin formation and degradation in n ephrosis, we measured fibrinopeptide A by radioimmunoassay 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/dI. Both fibrinopeptide A and D-dimer were abnorma lly elevated in the majority of nephrotics (P < 0.001 vs. healthy cont rols), providing evidence of increased fibrin generation and lysis ''i n vivo.'' A positive correlation was found between fibrinopeptide A an d 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 fi brinopeptide A, due to a reduction of in vivo thrombin activity. As en hanced thrombin activity can favor fibrin deposition within the renal parenchyma, as well as vascular complications, it is reasonable to ass ume that an antithrombotic treatment aimed at controlling thrombin gen eration may ameliorate the natural history of nephrosis.