ADMA/SDMA may be measured in individuals with multiple risk factors for the development of CVD.
SDMA is primarily excreted in the urine and identifies reduced renal function.
One of the earliest manifestations of endothelial dysfunction is nitric oxide (NO) deficiency, which promotes atherosclerosis. Asymmetric dimethylarginine (ADMA) and symmetric dimethylarginine (SDMA), its structural isomer, are metabolites of L-arginine, an amino acid that is catalyzed to L-citrulline and NO by nitric oxide synthase (NOS).
Both ADMA and SDMA have distinct pathophysiologies and manifestations. ADMA is a competitive inhibitor of NOS thereby reducing NO production and promoting endothelial dysfunction. SDMA also interferes with NO production, but does so indirectly by reducing the cellular availability of arginine. ADMA is primarily cleared through enzymatic degradation in the bloodstream and its presence identifies subclinical cardiovascular disease (CVD). Conversely, SDMA is primarily excreted in the urine and identifies reduced renal function.
Interpretation:
ADMA: Low // SDMA: Low
Normal endothelial function Med High Low
ADMA: Med / High // SDMA: Low
Endothelial dysfunction and possible presence of pre-diabetes/diabetes or CVD
ADMA: Low // SDMA: High
Reduced renal function
ADMA: Med / High // SDMA: High
- Endothelial dysfunction and possible presence of pre-diabetes/diabetes or CVD
- Reduced renal function
References:
American Diabetes Association Professional Practice Committee; 9. Pharmacologic Approaches to Glycemic Treatment: Standards of Medical Care in Diabetes—2022. Diabetes Care 1 January 2022; 45 (Supplement_1): S125–S143. https://doi.org/10.2337/dc22-S009
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