Heparin belongs to a class of compounds, the linear polyelectrolytes, that are miztures of carbohydrate chains with multiple acidic groups. Because these chains have a strong negative charge, they attach to cells rather than circulating in the plasma; they enter macrophages, the endothelium, cells of the reticuloendothelial system, and mast cells. Commercial heparin inhibits blood coagulation and prevents thrombus formation and platelet aggregation. Heparin also stimulates the release of lipoprotein lipase from endothelium, adipose tissue, and liver; modifies metabolism; inhibits DNA transformation; activates macrophages; and alters the activity of hormones and a wide range of enzymes.

Heparin is used primarily for preventing or reducing clot formation, but it has also been used for inflammatory and allergic conditions, for pain relief in burn patients, as an antiatherosclerotic agent, and as an antitumor agent in combination with cortisone. It is effective for managing unstable angina and has been shown to reduce the incidence of myocardial infarction in patients with refractory angina. In the SC formulation it has been shown to reduce the frquency and duration of anginal attacks and the number of episodes of silent ischemia. The SC formulation is attracting increasing attention because it is easy and convenient to use, does not require pumps, and generally causes less bleeding.

Recently researchers in Denmark and Netherlands reported that heparin may slow the progression of kidney disease in diabetic patients. They found that heparin given SC in low doses significantly reduced urinary alumin excretion in 39 diabetic patients with persistant urinary albumin excretion. Patients were randomly treated twice daily for 3 months with SC injections unfractionated heparin 5000IU, low molecular weight heparin 2000 IU, or isotonic aline. Both of the heparin preparations significantly reduced urinary albumin secretion. Twelve patients reported discomfort or bleeding at the injection sites; four patients dropped out of the trial.

Commercial heparin increases the ability of one of the heparinoids, heparin sulfate, which is found in the renal glomerular basement membrane. Heparan sulfate is involved in the glumerular permeability of large molecules. There appears to be a relation between albuminuria and glomerular membrane heparan sulfate in patients with diabetic nephropathy. Indeed, loss of heparan sulfate may contribute to the pathogenesis of diabetic nephropathy. In animal studies, heparin has been shown to prevent albuminuria and the thickening of the glomerular basement membrane and to improve proliferative glomerulonephritis.

According to Nolan et al., the ability of heparin to stimulate the synthesiss and sulfation of heparin sulfate in the glomerular membrane may induce structural changes in the extracellular matrix, which in turn may "prevent progression from incidents to overt nephropathy."