Cardiometabolic Disease Assessment (CMDA) Panel
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 |
||||||
Dyslipidemia |
Hyperglycemia |
Insulin resistance |
Hypertension |
Obesity |
Impaired kidney function |
Impaired liver function |
|
Atherosclerotic cardiovascular disease3,6-11 |
A |
O |
O |
O |
O |
O |
O |
Type 2 diabetes10,12-14 |
O |
A |
A |
O |
O |
O |
O |
Chronic kidney disease6,9,10,14,15 |
O |
O |
O |
O |
O |
A |
O |
Metabolic dysfunction-associated steatotic liver disease10,16 |
O |
O |
O |
O |
O |
O |
A |
Endocrine: |
|||||||
| Hypothyroidism6,10,11,17-20 |
O |
O |
S |
O |
O |
O |
I |
Primary aldosteronism21-23 |
I |
O |
S |
A |
O |
O |
O |
Hypogonadism/low testosterone10,24-26,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. Panelsa and Tests Included in the CMDA Panel
Test code |
Test name (component tests and codes) |
Method(s) |
Reference ranges for adultsb |
Glycemic control |
|||
Cardio IQ® Hemoglobin A1c |
Immunoturbidimetry |
|
|
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 |
|
|
Cardiovascular disease |
|||
Cardio IQ® Apolipoprotein B |
Immunoassay |
|
|
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 |
|
|
Endocrine disorder (thyroid) |
|||
TSH |
Immunoassay |
0.40-4.50 mIU/L |
|
Chronic kidney disease |
|||
Kidney Profile Includes albumin, random urine with creatinine (6517) and serum creatinine (375) with calculated eGFR. |
Turbidimetry, spectrophotometry |
|
|
MASLD |
|||
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 |
|
|
| 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:
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
- Martin SS, Aday AW, Allen NB, et al. 2025 Heart disease and stroke statistics: a report of US and global data from the American Heart Association. Circulation. 2025;151(8):e41-e660. doi:10.1161/CIR.0000000000001303
- Zhu F, Boersma E, Tilly M, et al. Trends in population attributable fraction of modifiable risk factors for cardiovascular diseases across three decades. Eur J Prev Cardiol. 2024;31(14):1724-1733. doi:10.1093/eurjpc/zwae219
- Arnett DK, Blumenthal RS, Albert MA, et al. 2019 ACC/AHA guideline on the primary prevention of cardiovascular disease: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on clinical practice guidelines. Circulation. 2019;140(11):e563-e595. doi:10.1161/CIRCULATIONAHA.0000000000000677
- Boersma P, Black LI, Ward BW. Prevalence of multiple chronic conditions among US adults, 2018. Prev Chronic Dis. 2020;17:E106. doi:10.5888/pcd17.200130
- Tian Y, Li D, Cui H, et al. Epidemiology of multimorbidity associated with atherosclerotic cardiovascular disease in the United States, 1999-2018. BMC Public Health. 2024;24(1):267. doi:10.1186/s12889-023-17619-y
- 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
- Nahmias A, Stahel P, Xiao C, et al. Glycemia and atherosclerotic cardiovascular disease: exploring the gap between risk marker and risk factor. Front Cardiovasc Med. 2020;7:100. doi:10.3389/fcvm.2020.00100
- 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
- Kidney Disease: Improving Global Outcomes (KDIGO) CKD Work Group. KDIGO 2024 clinical practice guideline for the evaluation and management of chronic kidney disease. Kidney Int. 2024;105(4S):S117-S314. doi:10.1016/j.kint.2023.10.018
- 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
- American Diabetes Association Professional Practice Committee. 10. Cardiovascular disease and risk management: standards of care in diabetes—2025. Diabetes Care. 2025;48(suppl 1):S207–S238. doi:10.2337/dc25-S010
- 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
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 |
||||||
Dyslipidemia |
Hyperglycemia |
Insulin resistance |
Hypertension |
Obesity |
Impaired kidney function |
Impaired liver function |
|
Atherosclerotic cardiovascular disease3,6-11 |
A |
O |
O |
O |
O |
O |
O |
Type 2 diabetes10,12-14 |
O |
A |
A |
O |
O |
O |
O |
Chronic kidney disease6,9,10,14,15 |
O |
O |
O |
O |
O |
A |
O |
Metabolic dysfunction-associated steatotic liver disease10,16 |
O |
O |
O |
O |
O |
O |
A |
Endocrine: |
|||||||
| Hypothyroidism6,10,11,17-20 |
O |
O |
S |
O |
O |
O |
I |
Primary aldosteronism21-23 |
I |
O |
S |
A |
O |
O |
O |
Hypogonadism/low testosterone10,24-26,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. Panelsa and Tests Included in the CMDA Panel
Test code |
Test name (component tests and codes) |
Method(s) |
Reference ranges for adultsb |
Glycemic control |
|||
Cardio IQ® Hemoglobin A1c |
Immunoturbidimetry |
|
|
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 |
|
|
Cardiovascular disease |
|||
Cardio IQ® Apolipoprotein B |
Immunoassay |
|
|
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 |
|
|
Endocrine disorder (thyroid) |
|||
TSH |
Immunoassay |
0.40-4.50 mIU/L |
|
Chronic kidney disease |
|||
Kidney Profile Includes albumin, random urine with creatinine (6517) and serum creatinine (375) with calculated eGFR. |
Turbidimetry, spectrophotometry |
|
|
MASLD |
|||
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 |
|
|
| 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:
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
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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
- Kidney Disease: Improving Global Outcomes (KDIGO) CKD Work Group. KDIGO 2024 clinical practice guideline for the evaluation and management of chronic kidney disease. Kidney Int. 2024;105(4S):S117-S314. doi:10.1016/j.kint.2023.10.018
- 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
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- 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
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- 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
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- 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
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Content reviewed 8/2025