ADMA/SDMA Test
The ADMA/SDMA test measures asymmetric and symmetric dimethylarginine, endogenous modulators of nitric oxide synthesis and renal clearance. ADMA inhibits nitric oxide synthase and reflects endothelial dysfunction; SDMA is renally cleared and detects early kidney impairment. Together they stratify cardiovascular risk and oxidative stress beyond traditional markers.
3
Biomarkers
Blood (serum)
Sample
5–7 business days
Turnaround
Yes
Fasting
What is the ADMA/SDMA test?
The ADMA/SDMA Test quantifies two endogenous dimethylarginines that modulate nitric oxide biology and renal clearance, offering a window into endothelial function, oxidative stress, and early renal impairment. Practitioners order this panel to stratify cardiovascular risk beyond traditional lipid and inflammatory markers, to detect subclinical endothelial dysfunction in metabolic syndrome or early-stage chronic kidney disease, and to personalise interventions targeting the nitric oxide pathway. ADMA and SDMA do not replace conventional risk scores or renal panels, but they quantify pathways that lipids and creatinine miss. The test is particularly valued in functional and preventive cardiology, where early detection of vascular dysfunction guides lifestyle, nutraceutical, and pharmaceutical strategies before structural disease emerges. Interpreting both analytes and their ratio together yields a richer assessment than either marker alone.
What does the ADMA/SDMA test measure?
Asymmetric dimethylarginine is an endogenous competitive inhibitor of nitric oxide synthase, formed when protein arginine methyltransferases methylate arginine residues in nuclear and cytoplasmic proteins and those proteins are subsequently proteolysed. It is metabolised primarily by dimethylarginine dimethylaminohydrolase enzymes (DDAH-1 and -2) and cleared to a lesser extent by renal excretion. Because it competes with L-arginine for the active site of nitric oxide synthase, elevated ADMA impairs endothelial nitric oxide production, reducing vascular relaxation and favouring endothelial dysfunction, vasoconstriction, and platelet aggregation.
ADMA is a functional marker of endothelial dysfunction and oxidative stress. Elevated concentrations predict cardiovascular events, stroke, and all-cause mortality in prospective cohort studies, and are implicated in the pathophysiology of hypertension, atherosclerosis, heart failure, chronic kidney disease, and insulin resistance. While not yet part of routine risk panels, ADMA quantifies the nitric oxide pathway disturbance that bridges metabolic and vascular disease.
Symmetric dimethylarginine is a structural isomer of ADMA, also formed from proteolysis of methylated proteins, but it does not inhibit nitric oxide synthase. Instead, SDMA is primarily cleared by the kidneys and its plasma concentration rises when glomerular filtration declines. It may interfere with arginine transport into endothelial cells, indirectly affecting nitric oxide production, and has emerged as a sensitive marker of renal function independent of creatinine.
SDMA serves as both a renal biomarker and a cardiovascular risk indicator. It correlates closely with estimated GFR and may detect early decline before creatinine rises, particularly in populations with preserved muscle mass or hyperfiltration. Elevated SDMA predicts progression of chronic kidney disease, cardiovascular events, and mortality, making it a complementary marker to creatinine and cystatin C in renal assessment and a functional cardiovascular-risk tool.
The ADMA/SDMA ratio reflects the balance between nitric oxide synthase inhibition (ADMA) and renal clearance capacity (SDMA). Because both dimethylarginines are produced via similar methylation and proteolysis pathways but cleared by different routes — ADMA mainly enzymatic, SDMA mainly renal — a rising ratio may signal disproportionate ADMA accumulation relative to renal function, suggesting enzymatic dysregulation or oxidative stress.
The ratio provides a functional snapshot of endothelial versus renal pathways. An elevated ratio may point to oxidative stress or DDAH impairment even when absolute ADMA is borderline, while a low ratio in the setting of elevated SDMA emphasises renal dysfunction. Interpreting the ratio alongside the absolute concentrations enriches the cardiovascular and metabolic picture.
Why is the ADMA/SDMA test ordered?
- Stratification of cardiovascular risk in patients with metabolic syndrome, insulin resistance, or early type 2 diabetes, particularly when traditional lipid panels are equivocal
- Assessment of endothelial function and oxidative stress in patients with hypertension, obesity, or a family history of premature atherosclerosis
- Detection of subclinical renal dysfunction in patients with preserved creatinine but clinical suspicion of early chronic kidney disease, hyperfiltration, or low muscle mass
- Monitoring patients on therapies targeting nitric oxide pathways, such as arginine or citrulline supplementation, antioxidants, or drugs affecting DDAH activity
- Investigation of unexplained cardiovascular symptoms or exercise intolerance where traditional markers do not fully explain the clinical picture
- Functional cardiology and longevity-focused assessment of vascular ageing and mitochondrial-endothelial health in asymptomatic patients seeking preventive optimisation
- Adjunctive evaluation in heart failure or chronic kidney disease to assess the interplay of nitric oxide impairment and renal clearance
Sample collection and turnaround
Sample type
Blood (serum)
Fasting required
Yes
Collection method
Venipuncture at patient service centre
Turnaround
5–7 business days
Collection notes
Phlebotomy at the processing laboratory's draw site (Quest, Boston Heart Diagnostics, or Access Medical Laboratories, depending on routing). Fasting for 10–12 hours is recommended to minimise postprandial variation in arginine and protein metabolism. Separate serum promptly and keep refrigerated or frozen if there is any delay.
Specimen requirements
Minimum 1.0 mL serum; gel separator acceptable. ADMA and SDMA are stable refrigerated for several days and frozen for months. Note the performing laboratory for serial comparability, as assay platforms and reference intervals differ.
What can affect ADMA/SDMA results?
Both ADMA and especially SDMA are renally cleared, so declining glomerular filtration raises plasma concentrations; SDMA rises more steeply than ADMA, lowering the ratio.
High-protein diets increase substrate for methylation and subsequent dimethylarginine release; acute arginine supplementation may transiently compete with ADMA at the nitric oxide synthase site but does not acutely lower plasma ADMA.
Inflammation, hyperglycaemia, and oxidative stress inhibit DDAH activity, reducing ADMA clearance and raising plasma ADMA disproportionately; this is a key mechanism linking metabolic disease to endothelial dysfunction.
Oestrogen upregulates DDAH and nitric oxide synthase, so premenopausal women and those on oestrogen replacement typically have lower ADMA; postmenopausal transition can unmask endothelial vulnerability.
Statins upregulate DDAH and improve endothelial function, lowering ADMA; antioxidants may reduce oxidative DDAH inhibition, though clinical effects are variable.
ADMA and SDMA are stable in serum but sensitive to pre-analytical factors; different platforms (ELISA, LC-MS/MS) yield different reference intervals, so results should be interpreted within the performing laboratory's range.
What do ADMA/SDMA results mean?
Elevated
Elevated ADMA reflects impaired nitric oxide synthesis and endothelial dysfunction, associated with increased cardiovascular risk, hypertension, atherosclerosis, insulin resistance, and oxidative stress. Elevated SDMA points primarily to declining renal clearance and early chronic kidney disease, though it also correlates with cardiovascular events. When both are raised, consider combined endothelial and renal pathology; a high ADMA:SDMA ratio suggests disproportionate nitric oxide synthase inhibition relative to renal function, flagging oxidative or metabolic stress.
Normal
Normal ADMA and SDMA suggest preserved endothelial nitric oxide production and renal clearance. However, normal results do not exclude cardiovascular disease if structural changes are already present, and longitudinal trends may reveal early drift before frank elevation.
Reduced
Low ADMA and SDMA are rarely pathological and may reflect excellent endothelial function, low oxidative stress, or high DDAH activity. Very low values in the context of malnutrition or severe hepatic dysfunction warrant correlation with clinical status, though this is uncommon.
Note: ADMA and SDMA are functional markers, not diagnostic tests. Reference intervals differ by assay and population, so absolute values must be interpreted within the laboratory's range. The ratio adds context but is not standardised. Elevated dimethylarginines predict risk in cohorts but are not yet incorporated into formal guidelines, so use them to guide individualised intervention rather than as standalone diagnostic criteria.
Frequently asked questions
ADMA is an endogenous inhibitor of nitric oxide synthase, impairing vascular relaxation and marking endothelial dysfunction. SDMA is a structural isomer that does not inhibit nitric oxide synthase but is primarily renally cleared, making it a sensitive marker of kidney function. Both are formed from protein methylation and degradation.
How to access the ADMA/SDMA test
The ADMA/SDMA reference page is free and open to all practitioners. Create a free practitioner account to see pricing, save tests to your list, and generate requisition forms. Verification takes 1–2 business days.
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Published: October 7, 2026
Last reviewed: October 7, 2026
- Böger RH, et al. Asymmetric dimethylarginine (ADMA): a novel risk factor for endothelial dysfunction — its role in hypercholesterolemia. Circulation. (1998)
- Schulze F, et al. Symmetric dimethylarginine predicts all-cause mortality following ischemic stroke. Atherosclerosis. (2010)
- Zoccali C, et al. Plasma concentration of asymmetrical dimethylarginine and mortality in patients with end-stage renal disease: a prospective study. Lancet. (2001)
- Schwedhelm E, Böger RH. The role of asymmetric and symmetric dimethylarginines in renal disease. Nature Reviews Nephrology. (2011)
- Kielstein JT, et al. Symmetric dimethylarginine (SDMA) as endogenous marker of renal function — a meta-analysis. Nephrology Dialysis Transplantation. (2006)
This content is for licensed healthcare practitioners only and does not constitute medical advice. Clinical decisions should be based on the full clinical picture and not on any single test result.
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