Chronic Kidney Disease 198 and plasma synthesized from endothelial cells (Figure 1). It is shown that high ADMA level increases the cardiovascular incident risk by 34% and mortality risk by 52% (4-8). Increased ADMA concentration has a high prevalence in hyperhomocysteinemia, coronary artery diseases, hypercholesterolemia, diabetes mellitus, hypertension, preeclampsia, peripheral arterial occlusive disease, impaired renal function and other diseases (7,9,10). Reduced nitric oxide (NO)-dependent vasodilation is regarded as an early indicator of atherosclerotic diseases (7,14). It is documented that adult patients with renal failure have 2-6 times higher ADMA than healthy subjects due to reduced renal excretion and reduced enzymatic degradation (15). NO is synthesized from L-arginine via NO synthase enzyme. NO inhibition decreases endothelial derived vasodilation and increases vascular resistance. Reduced NO availability can occur in patients with CKD. Moreover CKD can contribute to the accelaration of hypertension and cardiovascular complications. It appears that the increase in endogenic NO inhibitors like ADMA plays a major role in this process (11,(15)(16)(17). It has been shown that Hcy stimulates ADMA formation and plasma ADMA levels elevate in humans and animals by hyperhomocysteinemia (18)(19)(20). Increased serum Hcy level in adult CKD patients is an independent risk factor for cardiovascular system mortality. Elevated ADMA and hyperhomocysteinemia may be due to decreased renal excretion (18)(19)(20)(21)(22). It is reported that ADMA formation may be related with Hcy metabolism (18,19). It was found that there is a significant interaction of serum fibrinogen and CKD with respect to risk of both fatal/nonfatal coronary events and death (20-24).