Hypertension Workup

Updated: Feb 14, 2018
  • Author: Matthew R Alexander, MD, PhD; Chief Editor: Eric H Yang, MD  more...
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Approach Considerations

In general, the evaluation of hypertension primarily involves accurately measuring the patient’s blood pressure, performing a focused medical history and physical examination, and obtaining results of routine laboratory studies. [2, 3] A 12-lead electrocardiogram should also be obtained. These steps can help determine the following [2, 3, 4] :

  • Presence of end-organ disease

  • Possible causes of hypertension

  • Cardiovascular risk factors

  • Baseline values for judging biochemical effects of therapy

In an analysis of 4388 patients enrolled in the Coronary Artery Risk Development in Young Adults (CARDIA) study, a prediction model based on Framingham Heart Study criteria was better than prehypertension at identifying young adults who went on to develop new hypertension in the following 25 years. The c index for incident hypertension was 0.84 using the Framingham prediction model and 0.71 using prehypertension. [60, 61]

Criteria used in the CARDIA prediction model included age, sex, body mass index (BMI), smoking, systolic blood pressure (BP), and parental history of hypertension. Prehypertension was defined as systolic BP 120-139 mm Hg or diastolic BP 80-89 mm Hg.

Pulse wave velocity appears to have the potential to predict the progression of BP and development of hypertension in young adults (age 30-45 years). [201]


Baseline Laboratory Evaluation

Initial workup

Initial laboratory tests may include urinalysis; fasting blood glucose or A1c; hematocrit; serum sodium, potassium, creatinine (estimated or measured glomerular filtration rate [GFR]), and calcium; and lipid profile following a 9- to 12-hour fast (total cholesterol, high-density lipoprotein [HDL] cholesterol, low-density lipoprotein [LDL] cholesterol, and triglycerides). An increase in cardiovascular risk is associated with a decreased GFR level and with albuminuria. [2]

Assessment of suspected secondary causes

Other studies may be obtained on the basis of clinical findings or in individuals with suspected secondary hypertension and/or evidence of target-organ disease, such as complete blood count (CBC), chest radiograph, uric acid, and urine microalbumin. [2] Table 2, below, summarizes the Seventh Report of the Joint National Committee of Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7) screening tests for specific identifiable causes of hypertension.

Table 2. Identifiable Hypertension and Screening Tests (Open Table in a new window)


Screening Test

Chronic kidney disease

Estimated glomerular filtration rate

Coarctation of the aorta

Computed tomography angiography

Cushing syndrome; other states of glucocorticoid excess (eg, chronic steroid therapy

Dexamethasone suppression test

Drug-induced/drug-related hypertension*

Drug screening


24-hour urinary metanephrine and normetanephrine

Primary aldosteronism, other states of mineralocorticoid excess

Plasma aldosterone to renin activity ratio (ARR). If abnormal, refer for further evaluation such as saline infusion to determine if aldosterone levels can be suppressed, 24-hour urinary aldosterone level, and specific mineralocorticoid tests

Renovascular hypertension

Doppler flow ultrasonography, magnetic resonance angiography, computed tomography angiography

Sleep apnea

Sleep study with oxygen saturation (screening would also include the Epworth Sleepiness Scale [ESS])

Thyroid/parathyroid disease

Thyroid stimulating hormone level, serum parathyroid hormone level

Adapted from:  Chobanian AV, Bakris GL, Black HR, et al, and the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure; National Heart, Lung, and Blood Institute; National High Blood Pressure Education Program Coordinating Committee. Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Hypertension. Dec 2003;42(6):1206-52. [2]

* Some examples of agents that induce hypertension include nonsteroidal anti-inflammatory drugs (NSAIDs) and cyclooxygenase-2 (COX-2) inhibitors; illicit drugs; sympathomimetic agents; oral contraceptive or adrenal steroid hormones; cyclosporine and tacrolimus; licorice; erythropoietin; and certain over-the-counter dietary supplements and medicines, such as ephedra, ma huang, and bitter orange. Drug-related causes of hypertension may be due to nonadherence, inadequate doses, and inappropriate combinations.

Microalbuminuria is an early indication of diabetic nephropathy and is also a marker for a higher risk of cardiovascular morbidity and mortality. Recommendations suggest that individuals with type I diabetes should be screened for microalbuminuria. Usefulness of this screening in hypertensive patients without diabetes has not been established. [10]

Measurement of the ratio of aldosterone to plasma renin activity (PRA) is performed to detect evidence of primary hyperaldosteronism. A ratio of more than 20-30 is suggestive of this condition. Most antihypertensive medications can falsely raise or lower this ratio; thus, an appropriate washout period is necessary to obtain an accurate aldosterone-renin ratio.

As mentioned above, less than half of patients with PA have hypokalemia. However, an underlying secondary cause of hyperaldosteronism should be strongly suspected in patients with unprovoked hypokalemia or who exhibit an exaggerated hypokalemic response to a thiazide. It is important to note that aldosterone levels can be falsely low in the presence of hypokalemia. Hypokalemia and metabolic alkalosis are relatively late manifestations of primary hyperaldosteronism. A 24-hour urine specimen should be collected for sodium and potassium measurement. If the urine sodium level is more than 100 mmol/L and urine potassium is less than 30 mmol/L, hyperaldosteronism is unlikely.

If urinary potassium exceeds 30 mmol/L, the patient should have plasma renin activity measured. If the PRA is high, the likely cause is estrogen therapy, renovascular hypertension, malignant hypertension, or salt-wasting renal disease (or blockade of the renin-angiotensin system—the far more common reason). In the presence of low PRA, the serum aldosterone level can be measured (aldosterone and renin should be measured together; separate measurements will lead to inaccuracy). A low aldosterone level indicates licorice ingestion or other mineralocorticoid ingestion. A high aldosterone level indicates primary hyperaldosteronism. A computed tomography scan may identify the presence of an adenoma. In the absence of CT scan findings, differentiating hyperplastic hyperaldosteronism from adenoma is often difficult.

Determination of a sensitive thyroid-stimulating hormone (TSH) level excludes hypothyroidism or hyperthyroidism as a cause of hypertension.

If pheochromocytoma is suspected, urinary catecholamines and fractionated metanephrines are the tests of choice. Plasma fractionated metanephrines have specificity, but their sensitivity is too low for screening purposes. Urinary vanillylmandelic acid (VMA) is no longer recommended because of its poor sensitivity and specificity.

Evaluation of hypertensive emergencies

Electrolytes, blood urea nitrogen (BUN), and creatinine levels are used to identify renal impairment. A complete blood cell (CBC) count and smear help exclude microangiopathic anemia. Dipstick urinalysis can be used to detect hematuria or proteinuria (renal impairment), and microscopic urinalysis can be used to detect red blood cells (RBCs) or RBC casts (renal impairment). Optional studies include a toxicology screen, pregnancy test, and endocrine testing.


Radiologic Studies

If the patient’s history suggests renal artery stenosis and if a corrective procedure is considered, further noninvasive radiologic investigations (eg, computed tomographic angiography [CTA], magnetic resonance angiography [MRA]) or invasive renal angiography can be performed. [2, 3, 62] Concern over the risk of nephrogenic systemic fibrosis (NSF) due to gadolinium has reduced the use of MRA, particularly in patients with chronic kidney disease who have a glomerular filtration rate lower than 30 mL/min. This is a rare, debilitating, life-threatening disorder associated with gadolinium. CT or invasive angiography carries the risk of dye nephropathy.

For more information on NSF and contrast-induced nephropathy, see the US Food and Drug Administration (FDA) Web page Information on Gadolinium-Based Contrast Agents [63] and the American College of Radiology’s (ACR) Manual on Contrast Media (version 7).

Digital subtraction angiography

Digital subtraction angiography (DSA) with arterial injection of radiocontrast dye is the criterion standard for the evaluation of renal and pulmonary causes of hypertension, but this modality carries the risk of dye nephropathy and atheroemboli in patients with diabetes or chronic kidney disease. Captopril radionuclide scanning imaging technique does not give anatomic detail and is less often used, but this study can provide important information regarding the functionality of renal artery stenosis in the absence of advanced chronic kidney disease.


The main indication for echocardiography is evaluation for end-organ damage in a patient with borderline-high blood pressure (BP). Therefore, the presence of left ventricular hypertrophy (LVH) despite normal or borderline-high BP measurements requires antihypertensive therapy. Echocardiography may detect left atrial dilatation, LVH, and diastolic or systolic left ventricular dysfunction more frequently than electrocardiography. In addition, a stress echocardiogram can provide prognostic information in patients with hypertension and coronary artery disease (CAD). [64]