Serum concentrations of asymmetric (ADMA) and symmetric (SDMA) dimethylarginine in renal failure patients

Background. Nitric oxide (NO) synthesis is inhibited by the ADMA that accum ulates in the plasma of patients with renal failure, however, the concentra tion of SDMA also is enhanced. Therefore, it has been hypothesized that ADM A and SDMA may contribute to hypertension in these patients. Methods. We measured the concentrations of ADMA, SDMA and 21 endogenous ami no acids in 257 persons by high pressure liquid chromatography (HPLC). Results. The plasma concentrations of both ADMA and SDMA were significantly elevated in patients with chronic renal failure (CRF). The increase was mo re pronounced for SDMA (2.05 +/- 0.1 mu mol/L vs. 0.5 +/- 0.03 mu mol/L), w hereas it was only moderate for ADMA (0.85 +/- 0.03 mu mol/L vs. 0.73 +/- 0 .06 mu mol/L). In dialysis patients, the concentrations were further increa sed (ADMA, 1.05 +/- 0.04 mu mol/L; SDMA, 2.68 +/- 0.13 mu mol/L). After kid ney transplantation, the concentration of SDMA returned to the baseline val ue (1.15 +/- 0.11 mu mol/L), but that of ADMA remained enhanced (0.99 +/- 0 .06 mu mol/L). Conclusions. In CRF, especially the concentration of SDMA is significantly increased. Not only ADMA, but also SDMA are likely to be responsible for hy pertension. Competition for reabsorption between SDMA and arginine within t he kidney has to be considered fur the interpretation of changes in the rat io between dimethylarginines and arginine in renal failure. Hemodialysis is not suitable for a long-lasting removal of methylarginines. Whether the ad ministration of arginine could have promising effects on hypertension and c omplications of CRF needs to be studied in prospective trials.