Abstract
The etiology and clinical significance of hyperhomocysteinemia are under intense investigation. Although non-genetic ( 1) and genetic ( 2)( 3)( 4) factors influence plasma homocysteine concentrations, the etiology of moderate to intermediate hyperhomocysteinemia (15–50 μmol/L), commonly found in patients with coronary artery disease, cerebrovascular disease, peripheral vascular disease, and in patients with end-stage renal disease, is often unclear. The causes are likely to be multifactorial, involving both acquired and genetic components. There is strong evidence that hyperhomocysteinemia is an independent risk factor for cardiovascular disease ( 1)( 5)( 6)( 7), but there are conflicting reports as well ( 8)( 9)( 10). Some individuals cannot afford to wait the several years it may take before definitive results are available from intervention studies. These include patients with end-stage renal disease, renal transplant recipients, and heart transplant recipients. Immediate treatment of their hyperhomocysteinemia may be more prudent.