[Fibronectin].

The amino-terminal domain of fibronectin has a fibrin binding site and a site for covalent cross-linking to fibrin. This fibrin binding domain was isolated from human recombinant fibronectin and labeled with In-111; the final molecular weight was 12 kD. It was applied to a pilot study of 62 patients; 30 who were thought to have deep vein thrombosis and 32 controls. All 30 patients had either impedance plethysmography, duplex ultrasound, contrast venography, or various combinations of the three. Eight disagreements in the 30 patients suspected of having deep vein thrombosis were registered between fibrin binding domain imaging and the other examinations. Three of the patients with negative scan results had clots that were 1 week old or older, and this may be a limitation of the technique. In three other patients who had negative scan results, but positive alternative studies, there was a history of previous episodes of deep vein thrombosis and this could be a cause of false-positive results in the other modalities. There was one documented false-negative scan in a fresh clot. Normal scans were obtained in the lower extremities of the control patients, except in two who demonstrated uptake at the sites of insulin injections. The initial results of this feasibility study are encouraging and warrant further investigation.

Fibronectins↗

PubMed1992

Plasma fibronectin levels during acute rejection and acute tubular necrosis in renal transplant patients.

Fibronectin (Fn), an acute phase glycoprotein synthesized by the liver, has an important immunomodulatory role. We have investigated the changes in plasma Fn in patients after renal transplantation in order to determine whether these changes predict graft injury or rejection episodes. Besides normal healthy controls, healthy pregnant controls, and a trauma control group, we used two groups of chronic renal failure patients as controls: group I, patients with end-stage renal failure (ESRF) on peritoneal dialysis; group II, patients with ESRF on hemodialysis. These were compared with two groups of renal transplant patients: group III, patients 3 months after successful renal transplantation; group IV, patients studied sequentially 10 days immediately posttransplantation. The renal transplant patients were treated with low-dose cyclosporine, azathioprine, and steroids. Citrated plasma samples were collected for Fn assay by a sandwich-type ELISA and for SDS-PAGE analysis and Western blotting. The mean plasma Fn levels were as follows: healthy controls 311.6 SEM, 13.5 micrograms/ml; healthy pregnant controls 357 SEM, 5.9 micrograms/ml; trauma controls 262.3 SEM 31.7, micrograms/ml; group I 169 SEM, 25.1 micrograms/ml; group II 199 SEM, 27.2 micrograms/ml; group III 272 SEM, 21.7 micrograms/ml; group IV 212 SEM, 27.4 micrograms/ml (day 3 postop). There was a significant difference in the plasma Fn levels on day 3 posttransplant between the patients with delayed and immediate renal function (P less than 0.03) (group IV). A significant decrease in plasma Fn levels occurred immediately after steroid therapy was stopped (P less than 0.03) in patients treated for acute rejection. Plasma Fn levels were significantly decreased in the presence of delayed graft function but did not predict rejection.

Fibronectins↗