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

Abstract

Nitric oxide (NO) synthesis is inhibited by the ADMA that accumulates in the plasma of patients with renal failure; however, the concentration of SDMA also is enhanced. Therefore, it has been hypothesized that ADMA and SDMA may contribute to hypertension in these patients. We measured the concentrations of ADMA, SDMA and 21 endogenous amino acids in 257 persons by high pressure liquid chromatography (HPLC). The plasma concentrations of both ADMA and SDMA were significantly elevated in patients with chronic renal failure (CRF). The increase was more pronounced for SDMA (2.05 +/- 0.1 micromol/L vs. 0.5 +/- 0.04 micromol/L), whereas it was only moderate for ADMA (0.85 +/- 0.03 micromol/L vs. 0.73 +/- 0.06 micromol/L). In dialysis patients, the concentrations were further increased (ADMA, 1.05 +/- 0.04 micromol/L; SDMA, 2.68 +/- 0.13 micromol/L). After kidney transplantation, the concentration of SDMA returned to the baseline value (1.15 +/- 0.11 micromol/L), but that of ADMA remained enhanced (0.99 +/- 0.06 micromol/L). In CRF, especially the concentration of SDMA is significantly increased. Not only ADMA, but also SDMA are likely to be responsible for hypertension. Competition for reabsorption between SDMA and arginine within the kidney has to be considered for the interpretation of changes in the ratio between dimethylarginines and arginine in renal failure. Hemodialysis is not suitable for a long-lasting removal of methylarginines. Whether the administration of arginine could have promising effects on hypertension and complications of CRF needs to be studied in prospective trials.