Test Guide - Quest Test Directory

Cardiometabolic Disease Assessment (CMDA) Panel

This panel is used to assess cardiometabolic dysfunction in the context of (1) early-stage measures of dyslipidemia and glycemic control, (2) common endocrine disorders, and (3) downstream adverse effects on end-organ dysfunction, including liver and kidney.

Test Summary

Cardiometabolic Disease Assessment (CMDA) Panel

Test code: 14273

Clinical use

Identify early metabolic dysfunction in cardiometabolic disease in the context of measures of dyslipidemia and glycemic control
Assess common endocrine disorders that cause or are exacerbated by cardiometabolic dysfunction
Quantify downstream adverse effects of chronic cardiometabolic disease on end-organ dysfunction, including liver and kidney

Clinical background

Atherosclerotic cardiovascular disease (ASCVD) remains the leading cause of death in the United States,¹ although population-attributable risk factors have changed over time. Among other factors, smoking status, access to medications for dyslipidemia and hypertension, and prevalence of co-occurring type 2 diabetes (T2D) and obesity have changed, possibly reflected in the trends in ASCVD-attributable death over the decades.^2,3 Consequently, past factors may not best define risk for current and future cardiometabolic disease.

The complex interplay between multiple chronic diseases such as ASCVD, T2D, and other chronic kidney, liver, and endocrine diseases may also contribute to changes in ASCVD morbidity and mortality over time.Based on estimates using data from 2018, over half of adults (52%) in the United States had at least 1 chronic disease and more than a half of these adults (27% of all adults) had multiple chronic diseases.⁴ Data since 1999 indicate that ASCVD accounted for about 8% of the population with chronic disease, with declining prevalence except in those also affected by other chronic diseases.⁵ About two-thirds of patients with ASCVD had at least 4 additional chronic diseases.⁵ The complex interplay between chronic diseases is reflected in shared and varying degrees of association with related cardiometabolic conditions (Table 1).^3,6-29

Table 1. Chronic Diseases and Associated Conditions

Chronic disease or syndrome	Associated Conditions
Chronic disease or syndrome	Dyslipidemia	Hyperglycemia	Insulin resistance	Hypertension	Obesity	Impaired kidney function	Impaired liver function
Atherosclerotic cardiovascular disease^3,6-11	A	O	O	O	O	O	O
Type 2 diabetes^10,12-14	O	A	A	O	O	O	O
Chronic kidney disease^6,9,10,14,15	O	O	O	O	O	A	O
Metabolic dysfunction-associated steatotic liver disease^10,16	O	O	O	O	O	O	A
Endocrine:
Hypothyroidism^{6,10,11,17-20}	O	O	S	O	O	O	I
Primary aldosteronism^21-23	I	O	S	A	O	O	O
Hypogonadism/low testosterone^10,24-26,a	O	O	O	S	O	O	I
Polycystic ovary syndrome ^27-29,b,c	O	O	A	S	O	I	O

A, always or almost always associated (primary feature of the disease); O, often associated (most patients experience the condition); S, sometimes associated (some patients experience the condition); I, inconsistently associated (study results have been mixed). Degree of association based on current literature and guidelines.
^a	Men with type 2 diabetes or prediabetes and high atherosclerotic cardiovascular disease risk, chronic kidney disease, and low testosterone and should be screened for erectile dysfunction.¹⁶
^b	Classic polycystic ovary syndrome (PCOS) phenotypes A and B.²⁹
^c	Women with PCOS and hypertension during pregnancy are at risk for preeclampsia.²⁸

Quest Diagnostics offers the Cardiometabolic Disease Assessment (CMDA) Panel (test code 14273, Table 2)³⁰ to assess metabolic dysfunction in the context of

Glycemic control: hemoglobin A1c (HbA1c), C-peptide, insulin, and insulin resistance (IR) score
Cardiovascular disease: apolipoprotein B (apoB) and lipids (low density lipoprotein cholesterol [LDL-C], high density lipoprotein cholesterol [HDL-C], total cholesterol, triglycerides [TG])
Endocrine (thyroid) dysfunction: thyroid stimulating hormone (TSH) levels
Kidney dysfunction: estimated glomerular filtration rate (eGFR) and urine albumin-creatinine ratio (UACR)
Liver dysfunction: comprehensive metabolic panel with fibrosis-4 (FIB-4) index

Thus, the CMDA panel streamlines identification of disease progression of multiple cardiometabolic conditions through a single panel of tests.

Table 2. Panels^a and Tests Included in the CMDA Panel

Test code	Test name (component tests and codes)	Method(s)	Reference ranges for adults^b
Glycemic control
91732	Cardio IQ^® Hemoglobin A1c	Immunoturbidimetry	<5.7%
36509	Cardio IQ^® Insulin Resistance Panel with Scorec Includes Insulin, Intact LC/MS/MS (93103), C-peptided and calculated IR score.	High-throughput immunochemical enrichment, LC/MS/MS	C-peptide: 0.68-2.16 ng/mL Insulin: ≤16 μIU/mL
Cardiovascular disease
91726	Cardio IQ^® Apolipoprotein B	Immunoassay	<90 mg/dL
91716	Lipid Panel, Cardio IQ^® Includes total cholesterol (91717), triglycerides (91718), HDL-C (91719), calculated LDL-Ce cholesterol/HDL ratio, non-HDL-C, and Cardio IQ interpretive report.	Spectrophotometry	HDL-C: ≥50 mg/dL (female), ≥40 mg/dL (male) LDL-C, calc: <100 mg/dL non-HDL-C: <130 mg/dL TG: <150 mg/dL Total cholesterol: <200 mg/dL Total/HDL-C ratio: <5
Endocrine disorder (thyroid)
899	TSH	Immunoassay	0.40-4.50 mIU/L
Chronic kidney disease
39165	Kidney Profile Includes albumin, random urine with creatinine (6517) and serum creatinine (375) with calculated eGFR.	Turbidimetry, spectrophotometry	UACR: <30 mg/g creatinine Creatinine, random urine: 20-275 mg/dL Creatinine, serum: 0.5-1.03 mg/dL eGFR: ≥60 mL/min/1.73m2
MASLD
10372	Comprehensive Metabolic Panel With Fibrosis-4 (FIB-4) Index Includes albumin (223), albumin/globulin ratio (calculated), alkaline phosphatase (234), ALT (823), AST (822), BUN/creatinine ratio (296), calcium (303), carbon dioxide (310), chloride (330), creatinine with eGFR (375), globulin (calculated), glucose (483), potassium (733), sodium (836), total bilirubin (287), and total protein (754), urea nitrogen (294), platelet count (723), and FIB-4 index (calculated).	See individual tests	Alkaline phosphatase: 35-144 U/L ALT: 9-46 U/L AST: 10-35 U/L (males ≥50 years, females ≥45 years) Glucose: 65-99 mg/dL Platelet count: 140-400 thousand/μL Potassium: 3.5-5.3 mmol/L

ALT, alanine aminotransferase; AST, aspartate aminotransferase; BUN, blood urea nitrogen; Calc, calculated; eGFR, estimated glomerular filtration rate; HDL-C, high-density lipoprotein cholesterol; IR, insulin resistance; LC/MS/MS, liquid chromatography-tandem mass spectrometry; LDL-C, low-density lipoprotein cholesterol; MASLD, metabolic dysfunction-associated steatotic liver disease; TSH, thyroid stimulating hormone; UACR, urinary albumin-creatinine ratio.
^a	Panel components may be ordered separately with (as listed) or without enhanced reporting of CardioIQ risk categories: Hemoglobin A1c (test code 496), Apolipoprotein B (test code 5224), Lipid Panel, Standard (test code 7600).
^b	For IR score, see CardioIQ Insulin Resistance Panel With Score \| Test Summary \| Quest Diagnostics; for FIB-4 index, see Liver Fibrosis, Fibrosis-4 (FIB-4) Index Panel \| Test Summary \| Quest Diagnostics.
^c	This test was developed and its analytical performance characteristics have been determined by Quest Diagnostics. It has not been cleared or approved by FDA. This assay has been validated pursuant to the CLIA regulations and is used for clinical purposes.
^d	The C-peptide LC/MS/MS panel component cannot be ordered separately. C-peptide by immunoassay (test code 372) is not an equivalent test and cannot be used in calculation of the IR score.
^e	Calculated using the Martin-Hopkins calculation.³⁰

Early metabolic dysfunction

To identify early metabolic dysfunction, the CMDA panel uses measures of IR (IR score), HbA1c, apoB, and lipid testing to identify increasing cardiometabolic risk and potentially guide disease prevention efforts. A 2025 study has shown increasing prevalence of IR, apoB-LDL-C discordance (low LDL-C relative to apoB), vascular inflammation, and triglyceridemia, even within a population within the normal range of HbA1c.³¹ Another 2025 study demonstrated that normoglycemic individuals who developed incident prediabetes or T2D were characterized by higher and increasing IR scores when followed for 3 years compared with those that did not develop prediabetes or T2D, regardless of their age, sex, and overweight status.³²

If identifying early metabolic dysfunction is the primary objective, the Metabolic Risk Panel (test code 39447) also offers these test components.

Endocrine dysfunction

Endocrine diseases and syndromes can complicate the development and progression of cardiometabolic disease. Thus, the CMDA panel includes tests for TSH and polycystic ovary syndrome (PCOS) management:

TSH: Measuring TSH is important for identifying or excluding hypothyroidism as the primary cause of metabolic dysfunction, which can also manifest as impaired kidney function.¹⁹ Hypothyroidism/high TSH is also associated with cardiovascular conditions including bradycardia, pericardial effusion, decreased left ventricular function, diastolic hypertension, and weight gain due to a reduction in metabolic processes.¹⁹ Thus, the CMDA panel includes TSH as a direct measure of thyroid endocrine function (Table 2).

For more information regarding interpreting laboratory testing for thyroid dysfunction see Thyroid Dysfunction Laboratory Testing for Diagnosis and Management in Nonpregnant Adults.

PCOS and other endocrine disorders: While the CMDA panel contains no direct measures for diagnosis of PCOS and other endocrine disorders, the panel serves to measure metabolic dysfunction associated with these disorders:

For PCOS, the CMDA panel provides guideline-recommended testing for disease management for women who are overweight and obese, including a fasting lipid profile at diagnosis (total cholesterol, LDL-C, HDL-C, and TG level); thereafter, measurement should be guided by the results and the global CVD risk.²⁸
Quest separately offers tests to differentially diagnose PCOS (see Polycystic Ovary Syndrome: Laboratory Support of Diagnosis), diagnose primary aldosteronism (PA, see Plasma Renin Activity With Reflex to Aldosterone), and identify the cause of hypogonadism (see Hypogonadism and Low Testosterone in Men: Laboratory Support of Diagnosis and Management).

End-organ dysfunction

To quantify downstream adverse effects of chronic cardiometabolic disease on end-organ dysfunction, the CMDA panel includes guideline-recommended kidney⁹ and liver¹⁰ function laboratory testing (Table 2), in addition to assessing ASCVD risk and heart disease through lipid panels and apoB.³ This testing includes the Comprehensive Metabolic Panel With Fibrosis-4 (FIB-4) Index panel that evaluates metabolism and electrolyte balance within the body as well as kidney and liver function:

Kidney: The eGFR, which is calculated from serum creatinine, and UACR in the CMDA panel are recommended for annual CKD screening for patients starting at diagnosis of T2D by the American Diabetes Association (ADA) and the Kidney Disease: Improving Global Outcomes (KDIGO) group.⁹ Follow-up testing and treatment recommendations or referral to nephrology depend on the level of dysfunction assessed using the results of these tests in a Kidney Profile, which is incorporated in the CMDA panel.

For more information about CKD testing, see Laboratory Testing for Chronic Kidney Disease Diagnosis and Management | Test Guide | Quest Diagnostics

Liver: The FIB-4 index is a calculation based on age, aspartate aminotransferase (AST), alanine aminotransferase (ALT), and platelet count and is a sensitive marker of liver fibrosis. Both the American Association of Clinical Endocrinology (AACE) and American Association for the Study of Liver Diseases (AASLD) recommend that all patients with suspected metabolic dysfunction-associated steatotic liver disease (MASLD, formerly NAFLD) based on the presence of obesity, prediabetes, T2D, and metabolic risk factors should undergo primary risk assessment with the FIB-4 index.¹⁰

For more information about the FIB-4 index, see Liver Fibrosis, Fibrosis-4 (FIB-4) Index Panel | Test Summary | Quest Diagnostics. The AACE/AASLD also recommends screening children with obesity or T2D and adolescents with PCOS for MASLD using serum ALT.¹⁰

Given the high prevalence of risk factors for cardiometabolic disease in the US population, the CMDA panel has been designed for annual use by clinicians to assess the status of cardiometabolic disease in each patient. Follow-up testing during the year will be specific and responsive to those parameters that are abnormal in the annual panel.

Individuals suitable for testing

Individuals at risk of metabolic dysfunction (eg, individuals >45 years [male], >50 years [female], with family history of CVD, and/or with sedentary lifestyle)
Individuals at risk of IR, which can lead to prediabetes or T2D (eg, individuals who are overweight/obese [BMI >25, waist circumference: >35 inches, women; >40 inches, men]; have a family history of diabetes; have a history of gestational diabetes, or have acanthosis nigricans)
Individuals with an HbA1c ≥5.0%
Individuals with a history of hypertension
Individuals with endocrine disease (hypothyroidism, PA, hypogonadism/low-testosterone [low T], or PCOS)
Individuals with liver (MASLD) or kidney (CKD) disease

Methods

For panel components and methods used, see Table 2.

Interpretive information

Information for interpreting results for most tests included in the CMDA panel can be found in Test Guides that are available on the Test Directory. Whether values are in or out of range can be interpreted using Table 2. Extra information regarding the interaction between disorders in the context of the combined CMDA panel results is provided in Table 1 and below. This information is not intended as medical advice. Test interpretation, diagnosis, and patient management decisions should be based on the physician's education, clinical expertise, and assessment of the patient.

Early metabolic dysfunction

Results for HbA1c, TGs, LDL-C, total cholesterol/HDL-C, nonHDL-C, apoB, and the IR score are interpreted as “optimal,” “moderate,” or “high” in terms of cardiometabolic risk. Results for total cholesterol, HDL-C, glucose, intact insulin, and C-peptide are interpreted as “optimal” or “high” risk using single cutpoints. For more information, see the related Test Summary:

Metabolic Risk Panel | Test Summary | Quest Diagnostics

Endocrine dysfunction

Hypothyroidism

Results for TSH are interpreted as “optimal” or “high” for cardiometabolic risk, with high risk being indicated as a value above or below 2 cutpoints that define the reference range for apparently healthy adults (Table 2).

Increased TSH levels indicate hypothyroidism, increased insulin secretion,¹⁷ and can result in IR, although this may be more pronounced in normoglycemic people with subclinical hypothyroidism (increased TSH but in-range thyroid hormones FT3 and FT4),¹¹ and incidence of T2D may be higher in younger individuals (18-40 years).¹⁸ On the other hand, hyperglycemia is a common feature of both hypothyroidism (due to IR) and hyperthyroidism (low TSH and thus lower insulin secretion).¹⁷

Hypothyroidism is also associated with an atherogenic lipid profile,^6,19 including higher levels of LDL-C, apoB, TGs, and LDL particle number and size, which can be reversed with thyroid hormone therapy, although this reversal is less pronounced in subclinical hypothyroidism.³³

Hypothyroidism (TSH levels in the upper reference range or higher) and hyperthyroidism (TSH levels below the reference range) are also associated with kidney dysfunction and CKD progression.²⁰ The association with MASLD is less clear, with studies yielding inconsistent results.¹⁰

Primary aldosteronism (PA)

In PA patients, insulin secretion may be suppressed and clearance increased, leading to hyperglycemia.²² Consequently, these patients may not have elevated intact insulin and C-peptide levels or an elevated IR score. Compared with essential hypertension (EH), PA may have a stronger association with diabetes, although different studies indicate with varying degrees,^34,35 and a 2024 study suggests that PA may be less strongly associated with T2D.²³

Interestingly, compared to patients with EH, patients with PA had comparable risk of lipid disorders, which have been inconsistently associated with PA.²¹ Patients with PA are also at elevated risk of cardiovascular events, especially those whose renin activity remained suppressed (<1 μg/L/h) after treatment with mineralocorticoid receptor antagonists.^34,35

In addition, among other diagnoses, patients with PA also have higher risk of hypokalemia (odds ratio [OR], 3.5), fatty liver (OR, 1.9), CKD (OR, 1.6), obesity (OR, 1.4), and depression (OR, 1.4).²³

Hypogonadism (Low T)

In addition to higher rates of obesity, men with hypogonadism experience higher rates of IR and T2D.²⁴ The relationship is bidirectional in that hypogonadism and low T (eg, due to congenital defects, defects in the hypothalamic-pituitary-gonadal axis, or testicular damage) can cause metabolic effects, or metabolic effects may cause low T.

Low T is also associated with dyslipidemia²⁴ and hypertension.²⁵ In men undergoing testosterone replacement therapy (TRT), metabolically favorable changes including lower TGs, total cholesterol, and LDL-C may be observed. Low T also lowers HDL-C, which should be proatherogenic, but adverse CVD events have not been reproducibly demonstrated.³⁶ TRT has limited effects on glycemic control, and guidelines recommend against using TRT in men with T2D.³⁷

Low T is also associated with CKD; men with CKD frequently experience low testosterone levels, increasing CVD risk, morbidity, and mortality.²⁶ The association with MASLD is less clear, with studies yielding inconsistent results and requiring more research¹⁰

PCOS

Almost all women with PCOS have IR, which is one of the syndrome’s primary features.²⁸ They are at increased risk of metabolic dysfunction, although cardiometabolic profiles are worse for those with phenotypes A and B (classic PCOS) compared with phenotypes C (ovulatory PCOS) and D (nonhyperandrogenic PCOS)²⁷ Phenotypes A and B have higher BMI and waste circumference, worse IR, higher TGs, and lower HDLs compared with the other phenotypes.²⁷ Women under 40 years of age with PCOS have higher risks of developing prediabetes, T2D, and hypertension than their age-matched control individuals without PCOS.²⁷ Around perimenopause, compared with age-matched and BMI-matched control individuals, T2D and CVD risks appear similar for women with/without PCOS ²⁷

MASLD is prevalent in PCOS, even in lean women.²⁷ The association with kidney disease is less clear, with studies yielding inconsistent results and requiring more research.²⁹

End-organ dysfunction

Kidney

Results for serum creatinine and random urine creatinine are interpreted as “optimal” or “high” for cardiometabolic risk, with high risk being indicated as a value above or below 2 cutpoints that define the reference range for apparently healthy adults (Table 2). Results for eGFR and UACR are interpreted as “optimal” or “high” risk using single cutpoints.

The combined eGFR and UACR results from the Kidney Profile component of the CMDA panel will indicate whether treatment and/or referral to nephrology is warranted based on KDIGO guidelines.⁹ The combined measures capture early stage CKD when eGFR may be normal but albuminuria is present and UACR provides evidence of kidney damage.⁹ Individuals with CKD will also often have dyslipidemia, hypertension, hyperglycemia, IR, obesity, and/or MASLD.^6,9,10,14,15 CKD is also associated with T2D and ASCVD.^9,14

Liver

Results for the comprehensive metabolic panel are interpreted as “optimal” or “high” cardiometabolic risk for ALT, AST, glucose, and platelet count (above or below 2 cutpoints for each, Table 2) in addition to serum creatinine and eGFR (measured in the Kidney Profile). A FIB-4 index is interpreted as “optimal” “indeterminate/moderate,” or compatible with the presence of “advanced liver fibrosis” (>2.67).³⁸

MASLD is strongly associated with dyslipidemia, hypertension, obesity, and ASCVD, which is the leading cause of death for people with the condition.10 Individual markers correlate liver dysfunction to ASCVD to varying degrees. A large-scale study correlated ALT, AST, alkaline phosphatase, and gamma-glutamyl transferase levels with ASCVD in a multiethnic cohort.39 In addition, MASLD is strongly associated with hyperglycemia, IR, prediabetes,10 and T2D,16 and studies have shown that elevated intact insulin levels, measured and reported as part of the IR score, may be associated with MASLD, especially in young patients.40,41 Meta-analysis has indicated that patients with MASLD have double the prevalence of CKD and an 80% increased risk of incident CKD compared to patients without MASLD.10,42

References

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Pappan N, Awosika AO, Rehman A. Dyslipidemia. In: StatPearls [Internet]. StatPearls Publishing; 2025. Updated March 4, 2024, Accessed June 24, 2025. https://www.ncbi.nlm.nih.gov/pubmed/32809726
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Louie JZ, Shiffman D, McPhaul MJ, et al. Insulin resistance probability score and incident cardiovascular disease. J Intern Med. 2023;294(4):531-535. doi:10.1111/joim.13687
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Cusi K, Isaacs S, Barb D, et al. American Association of Clinical Endocrinology clinical practice guideline for the diagnosis and management of nonalcoholic fatty liver disease in primary care and endocrinology clinical settings: co-sponsored by the American Association for the Study of Liver Diseases (AASLD). Endocr Pract. 2022;28(5):528-562. doi:10.1016/j.eprac.2022.03.010
Yang W, Jin C, Wang H, et al. Subclinical hypothyroidism increases insulin resistance in normoglycemic people. Front Endocrinol (Lausanne). 2023;14:1106968. doi:10.3389/fendo.2023.1106968
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American Diabetes Association Professional Practice Committee. 2. Diagnosis and classification of diabetes: standards of care in diabetes—2025. Diabetes Care. 2025;48(suppl 1):S27–S49. doi:10.2337/dc25-S002
American Diabetes Association Professional Practice Committee. 11. Chronic kidney disease and risk management: standards of care in diabetes—2025. Diabetes Care. 2025;48(suppl 1):S239–S251. doi:10.2337/dc25-S011
Bishop NC, Burton JO, Graham-Brown MPM, et al. Exercise and chronic kidney disease: potential mechanisms underlying the physiological benefits. Nat Rev Nephrol. 2023;19(4):244-256. doi:10.1038/s41581-022-00675-9
American Diabetes Association Professional Practice Committee. 4. Comprehensive medical evaluation and assessment of comorbidities: standards of care in diabetes—2025. Diabetes Care. 2025;48(suppl 1):S59–S85. doi:10.2337/dc25-S004
Kalra S, Aggarwal S, Khandelwal D. Thyroid dysfunction and type 2 diabetes mellitus: screening strategies and implications for management. Diabetes Ther. 2019;10(6):2035-2044. doi:10.1007/s13300-019-00700-4
Sarabhai T, Kostev K. Thyroid disorders and the incidence of type 2 diabetes: insights from a 10-year cohort study in Germany. Endocr Connect. 2025;14(3)doi:10.1530/EC-24-0554
Chaker L, Razvi S, Bensenor IM, et al. Hypothyroidism. Nat Rev Dis Primers. 2022;8(1):30. doi:10.1038/s41572-022-00357-7
You AS, Kalantar-Zadeh K, Brent GA, et al. Impact of thyroid status on incident kidney dysfunction and chronic kidney disease progression in a nationally representative cohort. Mayo Clin Proc. 2024;99(1):39-56. doi:10.1016/j.mayocp.2023.08.028
Liang NP, Rao KR, Hu M, et al. The association between aldosterone and lipid profiles in patients with primary aldosteronism. Sci Rep. 2025;15(1):8755. doi:10.1038/s41598-025-92477-9
Adler GK, Murray GR, Turcu AF, et al. Primary aldosteronism decreases insulin secretion and increases insulin clearance in humans. Hypertension. 2020;75(5):1251-1259. doi:10.1161/HYPERTENSIONAHA.119.13922
Krieg A, Krieg S, Heuser A, et al. Exploring the spectrum of comorbidities associated with primary aldosteronism: insights from a large real-world case-control study. Biomedicines. 2024;12(11). doi:10.3390/biomedicines12112479
Miller C, Madden-Doyle L, Jayasena C, et al. Mechanisms in endocrinology: hypogonadism and metabolic health in men-novel insights into pathophysiology. Eur J Endocrinol. 2024;191(6):R1-R17. doi:10.1093/ejendo/lvae128
de Silva NL, Grant B, Minhas S, et al. Cardiovascular disease and testosterone therapy in male hypogonadism. Ann N Y Acad Sci. 2024;1540(1):121-132. doi:10.1111/nyas.15211
Zitzmann M. Testosterone deficiency and chronic kidney disease. J Clin Transl Endocrinol. 2024;37:100365. doi:10.1016/j.jcte.2024.100365
Helvaci N, Yildiz BO. Polycystic ovary syndrome as a metabolic disease. Nat Rev Endocrinol. 2025;21(4):230-244. doi:10.1038/s41574-024-01057-w
Teede HJ, Tay CT, Laven JJE, et al. Recommendations from the 2023 international evidence-based guideline for the assessment and management of polycystic ovary syndrome. J Clin Endocrinol Metab. 2023;108(10):2447-2469. doi:10.1210/clinem/dgad463
Peng H, Ren J, Zhao Y, et al. Unraveling the connection between PCOS and renal complications: current insights and future directions. Diabetes Res Clin Pract. 2025;224:112235. doi:10.1016/j.diabres.2025.112235
Martin SS, Blaha MJ, Elshazly MB, et al. Comparison of a novel method vs the Friedewald equation for estimating low-density lipoprotein cholesterol levels from the standard lipid profile. JAMA. 2013;310(19):2061-2068. doi:10.1001/jama.2013.280532
Penn MS, Winchester TB, Saghir J, et al. Cardiometabolic disease associated markers increase at an A1C >5%. Presented at: National Lipid Associations; 2025 Annual Scientific Sessions; May 29-June 1, 2025; Miami, FL.
Louie JZ, Shiffman D, Melander M, et al. Among those with normoglycemia, insulin resistance risk score (IRRS) elevation is observed up to 3 years prior to diagnosis of diabetes or prediabetes. Presented at: American Diabetes Association 85th Scientific Sessions; June 20-23, 2025; Chicago, IL.
Cappola AR, Desai AS, Medici M, et al. Thyroid and cardiovascular disease: research agenda for enhancing knowledge, prevention, and treatment. Circulation. 2019;139(25):2892-2909. doi:10.1161/CIRCULATIONAHA.118.036859
Monticone S, D'Ascenzo F, Moretti C, et al. Cardiovascular events and target organ damage in primary aldosteronism compared with essential hypertension: a systematic review and meta-analysis. Lancet Diabetes Endocrinol. 2018;6(1):41-50. doi:10.1016/S2213-8587(17)30319-4
Hundemer GL, Curhan GC, Yozamp N, et al. Cardiometabolic outcomes and mortality in medically treated primary aldosteronism: a retrospective cohort study. Lancet Diabetes Endocrinol. 2018;6(1):51-59. doi:10.1016/S2213-8587(17)30367-4
Snyder PJ, Bhasin S, Cunningham GR, et al. Lessons from the testosterone trials. Endocr Rev. 2018;39(3):369-386. doi:10.1210/er.2017-00234
Bhasin S, Brito JP, Cunningham GR, et al. Testosterone therapy in men with hypogonadism: an endocrine society clinical practice guideline. J Clin Endocrinol Metab. 2018;103(5):1715-1744. doi:10.1210/jc.2018-00229
Tapper EB, Lok AS. Use of liver imaging and biopsy in clinical practice. N Engl J Med. 2017;377(8):756-768. doi:10.1056/NEJMra1610570
Wang Y, Zhang Z, Ren W, et al. Liver function differences in atherosclerotic cardiovascular disease: a multi-ethnic dual-cohort retrospective study. Front Endocrinol (Lausanne). 2025;16:1558872. doi:10.3389/fendo.2025.1558872
Bril F, McPhaul MJ, Kalavalapalli S, et al. Intact fasting insulin identifies nonalcoholic fatty liver disease in patients without diabetes. J Clin Endocrinol Metab. 2021;106(11):e4360-e4371. doi:10.1210/clinem/dgab417
Huneault HE, Lo JS, Bai S, et al. Fasting intact insulin by mass spectrometry is associated with metabolic dysfunction-associated steatotic liver disease in youth. Hepatol Commun. 2024;8(12)doi:10.1097/HC9.0000000000000582
Musso G, Gambino R, Tabibian JH, et al. Association of non-alcoholic fatty liver disease with chronic kidney disease: a systematic review and meta-analysis. PLoS Med. 2014;11(7):e1001680. doi:10.1371/journal.pmed.1001680

Content reviewed 8/2025

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This is the most common Lipid Panel. Components include those useful in the detection, classification, and monitoring of patients with hyperlipidemia.

36509 - Cardio IQ® Insulin Resistance Panel with Score

The determination of insulin in serum is primarily used for the diagnosis of glycemic disorders in diabetic and pre-diabetic patients in the assessment of insulin resistant syndromes. Insulin is synthesized by the pancreatic beta cell as a precursor, proinsulin. Proinsulin is processed to insulin and C-peptide, a contiguous peptide between the insulin A and B chains, as it passes through the cell. The C-peptide in the proinsulin ensures correct folding and processing of proinsulin as it passes through the cell. Both insulin and C-peptide are released together from the beta cells in response to increased glucose levels. Because of differences in half-life and hepatic clearance, peripheral blood levels of C-peptide and insulin are no longer equimolar but remain highly correlated. A steady-state plasma glucose test in individuals undergoing an insulin suppression test to assess insulin resistance found that the combination of insulin and C-peptide was a better indicator of insulin resistance than either one individually.

14273 - Cardiometabolic Disease Assessment (CMDA) Panel

This panel combines tests used in the diagnosis and management of cardiometabolic disease elements, including metabolic syndrome, prediabetes, diabetes, thyroid conditions, kidney, fatty liver, and cardiovascular disease risk.

The benefits of GLP-1 therapies extend far beyond glycemic control and weight reduction.[1] These agents provide cardiovascular benefits, showing promise in improving kidney and liver health while on GLP-1 treatment.[1] This panel can establish a baseline prior to initiating GLP-1 therapy, if clinically indicated and a periodic comprehensive view of a patient’s cardiometabolic health thereafter. Note this panel does not measure Glucagon-like peptide-1 hormone levels in blood.

Up to 45% of Americans have a chronic disease; more than half of older adults have multiple chronic conditions.[2] The related chronic cardiometabolic conditions are characterized by initial stages that may remain clinically silent for years.

Medical societies, like the American Heart Association, recognize the interrelated impacts of metabolic risk factors (e.g., obesity and diabetes), chronic kidney disease (CKD), and cardiovascular disease, and the gap in early screening, prevention, and management of these chronic conditions.[3,4] Rising rates of metabolic dysfunction, obesity, and type 2 diabetes mellitus (T2DM) also contribute to increased prevalence of nonalcoholic fatty liver disease (NAFLD), also known as metabolic dysfunction-associated steatotic liver disease (MASLD).[5] Thyroid health may either be impacted by or exacerbate cardiometabolic conditions, such as coronary heart disease (CHD), MASLD, and CKD.[6-9]

The Cardiometabolic Disease Assessment Panel includes guideline-recommended testing that spans interrelated areas of cardiometabolic disease to determine the extent of metabolic dysfunction (glycemic control and advanced lipid assessment), identify whether thyroid health contributes to or is altered by metabolic dysfunction, and adverse impacts to heart, liver, and kidney function.[10-14] Identification of cardiometabolic disease presence can help guide personalized treatment strategies to prevent or delay disease progression and related complications.

This panel should be requested when all elements are medically necessary, and components have not recently been reported. The results of this panel should be interpreted in the context of pertinent clinical and family history and physical examination findings.

References
1. Rosen C, et al. N Engl J Med. 2026;394:1313-1324. doi: 10.1056/NEJMra2500106.
2. Raghupathi W, et al. Int J Environ Res Public Health. 2018;15(3):431. doi:10.3390/ijerph15030431.
3. Ndumele CE, et al. Circulation. 2023;148(20):1636-1664. doi.org/10.1161/CIR.0000000000001186.
4. Khan SS, et al. Circulation. 2024;149(6):430-449. doi: 10.1161/CIRCULATIONAHA.123.067626.
5. Bril F, et al. J Clin Endocrinol Metab. 2021;106(11):e4360-e4371. doi:10.1210/clinem/dgab417.
6. Cappola AR, et al. Circulation. 2019;139(25):2892- 2909. doi.org/10.1161/circulationaha.118.036859.
7. Kalra S, et al. Diabetes Ther. 2019;10(6):2035-2044. doi:10.1007/s13300-019-00700-4.
8. Mantovani A, et al. Thyroid. 2018;28(10):1270-1284. doi:10.1089/ thy.2018.0257.
9. Iglesias P, et al. Rev Endocr Metab Disord. 2017;18(1):131-144. doi:10.1007/s11154-016-9395-7.
10. Classification and Diagnosis of Diabetes: Standards of Medical Care in Diabetes-2020. Diabetes Care. 2020;43(Suppl 1):S14-S31. doi: 10.2337/dc23-S002.
11. Arnett DK, et al. J Am Coll Cardiol. 2019. doi: 10.1161/CIR.0000000000000677.
12. Cusi K, et al. Clinical Practice Guidelines. 2022;28(5):P528-562. doi:10.1016/j.eprac.2022.03.010.
13. Rinella NE, et al. Hepatology. 2023;77(5):1797-1835. doi:10.1097/HEP.0000000000000323.
14. Kidney Disease: Improving Global Outcomes (KDIGO) CKD Work Group. Kidney Int. 2024;105(4S):S117-S314. doi:10.1016/j.kint.2023.10.018.

91726 - Cardio IQ® Apolipoprotein B

Apolipoprotein B (APO B) has been reported to be a powerful indicator of CAD. In some patients with CAD, APO B is elevated even in the presence of normal LDL cholesterol.

496 - Hemoglobin A1c

To assist with control of blood glucose levels, the American Diabetes Association (ADA) has recommended glycated hemoglobin testing (HbA1c) twice a year for patients with stable glycemia, and quarterly for patients with poor glucose control. Interpretative ranges are based on ADA guidelines.

10372 - Comprehensive Metabolic Panel with Fibrosis-4 (FIB-4) Index

The FIB-4 index is a simple non-invasive approach using selected laboratory measures (AST, ALT, platelet count) in combination with patient age to assess if an individual is at higher risk for advanced liver fibrosis (F3-F4).

7600 - Lipid Panel, Standard

The Lipid Panel, Standard measures serum cholesterol and triglyceride (TG) levels; it includes evaluation of the cholesterol/HDL-C ratio (calculated), HDL-C, LDL-C (calculated), non-HDL-C (calculated), total cholesterol, and TG. Comprehensive lipid assessment aids in the evaluation of cardiovascular risk and the likelihood of suffering an ischemic event. It is also useful for the prevention and management of atherosclerotic disease, as well as the diagnosis of metabolic syndrome [1].

Cardiovascular disease (CVD) is the leading cause of death in the United States. The risk of developing CVD and having an ischemic event is significantly increased in individuals with high LDL-cholesterol (LDL-C) and TG levels [2,3]. The American Heart Association (AHA) recommends that Americans aged 20 and above have their lipid levels tested every 4 to 6 years. Children should have their cholesterol tested for the first time between ages 9 and 11, and again between ages 17 and 21. Testing should start earlier if there is family history of high cholesterol [4].

The AHA recommends repeat measurement of LDL-C within 4 to 12 weeks of starting or changing lipid-lowering therapy, to assess response and adherence, and then every 3 to 12 months as appropriate [4].

Treatment with N-acetyl cysteine (NAC) for acetaminophen overdose may generate a falsely low result for cholesterol. Venipuncture immediately after or during administration of the painkiller metamizole (dipyrone) may also lead to falsely low results for cholesterol.

Note: Any or all individual tests from a panel can be ordered separately.

References
1. Stone NJ, et al. Circulation. 2014;129(suppl 2):S1-S45.
2. CDC. Heart disease fact sheet. Reviewed August 23, 2017.
https://www.cdc.gov/dhdsp/data_statistics/fact_sheets/fs_heart_disease.htm
3. Arbel Y, et al. Card Diabetol. 2016;15:11.
4. AHA. Cholesterol management guide for healthcare practitioners. November 10, 2018.
https://www.heart.org/-/media/files/health-topics/cholesterol/chlstrmngmntgd_181110.pdf

91732 - Cardio IQ® Hemoglobin A1c

899 - TSH

For differential diagnosis of primary, secondary, and tertiary hypothyroidism. Also useful in screening for hyperthyroidism. This assay allows adjustment of exogenous thyroxine dosage in hypothyroid patients and in patients on suppressive thyroxine therapy for thyroid neoplasia.

Related guides (8)

Thyroid Dysfunction in Nonpregnant Adults

This Clinical Focus discusses the role that laboratory testing plays in the diagnosis and management of thyroid dysfunction in nonpregnant adults.

Laboratory Testing for Diabetes Diagnosis, Risk Assessment, and Management

This test guide discusses the use of laboratory tests for general screening and diagnosis of prediabetes and diabetes; it also provides additional information on diabetes risk assessment and monitoring glycemic control and complications in individuals with diabetes.

Laboratory Testing for Chronic Kidney Disease Diagnosis and Management

This test guide provides an overview of tests used to detect chronic kidney disease (CKD) in adults, as well as monitor CKD progression, comorbidities, complications, and response to therapy.

Liver Fibrosis, Fibrosis-4 (FIB-4) Index Panel

This test is used to assess the likelihood of advanced liver fibrosis.

Metabolic Risk Panel

This panel is used to assess early metabolic dysfunction and cardiometabolic risk.

Polycystic Ovary Syndrome (PCOS)

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Plasma Renin Activity With Reflex to Aldosterone

This test is used to screen for primary aldosteronism.

Hypogonadism and Low Testosterone in Men: Laboratory Support of Diagnosis and Management

This Clinical Focus describes approaches to testing for the diagnosis of low testosterone and monitoring during testosterone therapy in men with hypogonadism. Details of available tests are provided, as well as information about interpreting test results.

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Reference ranges are provided as general guidance only. To interpret test results use the reference range in the laboratory report.

The tests listed by specialty and category are a select group of tests offered. For a complete list of Quest Diagnostics tests, please adjust the filter options chosen, or refer to our Directory of Services.