SDMA is formed by methylation of protein l-arginine (L-Arg) residues in vivo; it is largely eliminated by renal clearance. In contrast to ADMA, it is not a direct inhibitor of nitric oxide synthase (NOS).
SDMA is a reliable marker of renal function (2), equals cystatin C in this respect, but outperforms serum creatinine. It is not influenced by muscle mass, diet, inflammation, diabetes, and is only slightly affected by obesity, age and
Should be measured in combination with ADMA, and a marker of renal function.
Patient/subject: SDMA concentration is unaffected by most diets.
Matrix: EDTA plasma and serum.
Volume: Minimum volume is 50 µL, but 200 µL is optimal and allows reanalysis.
Preparation: The blood sample must be centrifuged and the plasma/serum fraction put on ice, and frozen.
Reported values: 0.3-0.7 µmol/L.
Intraclass correlation coefficient (ICC): 0.62.
1. Midttun, O., Kvalheim, G., and Ueland, P.M. (2013). High-throughput, low-volume, multianalyte quantification of plasma metabolites related to one-carbon metabolism using HPLC-MS/MS. Anal Bioanal Chem 405, 2009-017.
2. Kielstein, J.T., Salpeter, S.R., Bode-Boeger, S.M., Cooke, J.P., and Fliser, D. (2006). Symmetric dimethylarginine (SDMA) as endogenous marker of renal function–a meta-analysis. Nephrol Dial Transplant 21, 2446-451.
3. El-Khoury, J.M., Bunch, D.R., Hu, B., Reineks, E.Z., and Wang, S. (2016). Comparison of symmetric dimethylarginine with creatinine, cystatin C and their eGFR equations as markers of kidney function. Clin Biochem 49, 1140-43.