In vivo measurements of fibrin formation and degradation in nephrotic patients.
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 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/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.
Sagripanti
A
A
1st Clinical Medicine Institute, University Hospital, Pisa, Italy.
Cupisti
A
A
Baicchi
U
U
Ferdeghini
M
M
Barsotti
G
G
D000293:Adolescent; D000328:Adult; D000368:Aged; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005338:Fibrin Fibrinogen Degradation Products / Q000032:analysis*; D005344:Fibrinopeptide A / Q000032:analysis*; D006493:Heparin / Q000627:therapeutic use; D006801:Humans; D008297:Male; D008875:Middle Aged; D009404:Nephrotic Syndrome / Q000097:blood* / Q000188:drug therapy
D005338:Fibrin Fibrinogen Degradation Products; C036309:fibrin fragment D; D005344:Fibrinopeptide A; C006871:calcium heparin; D006493:Heparin