SDMA

Optimal result: 73 – 135 ng/mL

Elevated SDMA levels positively correlate with reduced renal function, as measured by estimated glomerular filtration rate and cystatin C.

Interpretation:

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

What is the endothelium and why is it important?

The endothelium is a thin layer of cells lining the inside of your blood vessels. These cells are in constant contact with the blood supply and, therefore, play an integral role in immunity, blood clotting and maintenance of blood pressure. When your endothelium is damaged, it may signify that you are at increased risk of having cardiovascular disease or renal failure.

What are ADMA and SDMA?

ADMA (asymmetric dimethylarginine) and SDMA (symmetric dimethylarginine) are compounds made in your body as proteins are degraded, or broken down. ADMA and SDMA reduce your body’s ability to produce nitric oxide, a molecule that helps maintain a healthy endothelium.

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/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.

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

SDMA
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