The adverse effect of hyperhomocysteinemia on vascular wall can partially be explained by increasing plasma concentration of asymmetric dimethylarginine (ADMA), a potent inhibitor of nitric oxide synthase. The aim of the study was to compare ADMA and homocysteine levels in three groups of 40 subjects: I) blood donors with normal homocysteine (mean homocysteine 10.4 ± 3.4 µmol/l), II) patients with hyperhomocysteinemia and normal kidney function (mean homocysteine 15.4 ± 4.2 µmol/l) and III) hemodialysis patients who are known to be hyperhomocysteinemic (mean homocysteine 29.3 ± 13.0 µmol/l). Homocysteine (enzymatic method, Carolina, USA), ADMA (ELISA, DLD Diagnostika, Germany) and creatinine (Jaffé method) in EDTA plasma were measured. Plasma ADMA levels were significantly higher in both groups with hyperhomocysteinemia (1.59 ± 0.56 µmol/l in group II, 1.84 ± 0.57 µmol/l in group III) when compared with those in blood donors (0.82 ± 0.30 µmol/l, P < 0.001 in both cases). Significant correlations were found between ADMA and homocysteine (r = 0.42, P < 0.0001), ADMA and creatinine (r = 0.41, P < 0.0001), homocysteine and creatinine (r = 0.69, P < 0.0001). Increased ADMA concentration in hyperhomocysteinemic patients was confirmed. Although there exists a positive correlation between ADMA and creatinine, markedly increased ADMA concentration in hyperhomocysteinemic patients with normal creatinine concentration shows that homocysteine determines ADMA levels rather than kidney function.

        Key words: asymmetric dimethylarginine, homocysteine, hemodialysis, hyperhomocysteinemia.