No effect of unfractioned or low molecular weight heparin treatment on markers of vascular wall and hemostatic function in incipient diabetic nephropathy.
OBJECTIVE
The high risk for cardiovascular disease in IDDM patients with nephropathy may be mediated by abnormal function of the vascular wall. We investigated whether heparin was able to modulate markers of vascular wall and hemostatic function in patients with incipient nephropathy.


METHODS
Thirty-five IDDM patients with incipient nephropathy were randomized to treatment with placebo, unfractioned heparin, or low molecular weight heparin in a double-blind trial. The treatment was given as 1 h of conventional intravenous high-dose treatment and in a conventional subcutaneous low-dose regime for 3 months. Transcapillary escape rate of albumin and plasma levels of von Willebrand factor, fibrinogen, prothrombin fragment 1 + 2, thrombin-antithrombin III complexes, tissue type plasminogen activator, tissue plasminogen activator inhibitor type 1, total cholesterol, HDL cholesterol, and triglycerides were measured before and after treatment. Of the patients, 31 completed the study.


RESULTS
We found no significant effect of heparin on markers of vascular wall and hemostatic function by any of the treatments.


CONCLUSIONS
Treatment with high- or low-dose heparin induced no modulation of markers of vascular wall or hemostatic function in IDDM patients with incipient diabetic nephropathy.
Myrup
B
B
Steno Diabetes Center, Gentofte, The Netherlands.
Jensen
T
T
Gram
J
J
Kluft
C
C
Jespersen
J
J
Deckert
T
T
D000328:Adult; D000419:Albuminuria; D000990:Antithrombin III / Q000032:analysis; D002196:Capillaries / Q000187:drug effects / Q000503:physiopathology; D002318:Cardiovascular Diseases / Q000517:prevention & control; D002784:Cholesterol / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood; D003922:Diabetes Mellitus, Type 1 / Q000097:blood / Q000503:physiopathology*; D003925:Diabetic Angiopathies / Q000453:epidemiology / Q000517:prevention & control; D003928:Diabetic Nephropathies / Q000097:blood / Q000503:physiopathology*; D004311:Double-Blind Method; D005260:Female; D005340:Fibrinogen / Q000032:analysis; D006487:Hemostasis / Q000187:drug effects*; D006493:Heparin / Q000494:pharmacology*; D006495:Heparin, Low-Molecular-Weight / Q000494:pharmacology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000503:physiopathology; D010446:Peptide Fragments / Q000032:analysis; D010447:Peptide Hydrolases / Q000032:analysis; D010919:Placebos; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D011498:Protein Precursors / Q000032:analysis; D011516:Prothrombin / Q000032:analysis; D010959:Tissue Plasminogen Activator / Q000097:blood; D014280:Triglycerides / Q000097:blood; D014841:von Willebrand Factor / Q000032:analysis
D008076:Cholesterol, HDL; D006495:Heparin, Low-Molecular-Weight; D010446:Peptide Fragments; D010919:Placebos; D017395:Plasminogen Activator Inhibitor 1; D011498:Protein Precursors; D014280:Triglycerides; C046193:antithrombin III-protease complex; D014841:von Willebrand Factor; C029733:prothrombin fragment 1; C044183:prothrombin fragment 2; D000990:Antithrombin III; D011516:Prothrombin; D005340:Fibrinogen; D006493:Heparin; D002784:Cholesterol; D010447:Peptide Hydrolases; D010959:Tissue Plasminogen Activator