Secondary Hypertension

Article Author:
Sharana Hegde

Article Editor:
Narothama Aeddula

Editors In Chief:
Sisira Reddy
Joseph Nahas
Chokkalingam Siva

Managing Editors:
Avais Raja
Orawan Chaigasame
Khalid Alsayouri
Kyle Blair
Radia Jamil
Erin Hughes
Patrick Le
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Saad Nazir
William Gossman
Hassam Zulfiqar
Navid Mahabadi
Hussain Sajjad
Steve Bhimji
Muhammad Hashmi
John Shell
Matthew Varacallo
Heba Mahdy
Ahmad Malik
Sarosh Vaqar
Mark Pellegrini
James Hughes
Beenish Sohail
Hajira Basit
Phillip Hynes
Sandeep Sekhon

11/14/2019 9:37:51 PM


Hypertension affects about 30% of adults in the United States.[1] Most cases are due to essential hypertension, i.e., hypertension without an identifiable cause. But, about 5 to 10% of cases of hypertension are due to secondary hypertension.[2]

Secondary hypertension is elevated blood pressure (BP), which is secondary to an identifiable cause. Since its prevalence is relatively low, performing routine evaluations in every case of hypertension is not cost effective and is also time-consuming. However, one must be aware of clinical clues that could suggest a secondary cause of hypertension. The clinical clues to look out for that could be suggestive of a secondary cause of hypertension are as follows[3]:

  • Resistant hypertension, i.e., persistent blood pressure greater than 140/90 mm Hg despite using three anti-hypertensives from different classes, that includes a diuretic, all at adequate doses.
  • Increased lability or acute rise in blood pressure in a patient who had previously stable pressures.
  • Hypertension that develops in non-black patients less than 30 years of age, who do not have any other risk factors for hypertension, e.g., obesity, family history, etc.
  • Patients with severe hypertension (BP greater than 180/110 mm Hg) and patients with end-organ damage like acute kidney injury, neurological manifestations, flash pulmonary edema, hypertensive retinopathy, left ventricular hypertrophy, etc.
  • Hypertension that is associated with electrolyte disorders like hypokalemia or metabolic alkalosis
  • Age of onset of hypertension before puberty.
  • Non-dipping or reverse dipping presents while monitoring 24-hour ambulatory blood pressure. (Normally, the blood pressure at night is lower than the blood pressure during the day, i.e., there is a ‘dip’ in blood pressure at night. The absence of this ‘dip’ or ‘reverse dipping,’ i.e., ‘dip’ present during the day instead of at night can be suggestive of a secondary cause of hypertension).


The etiology of secondary hypertension is varied. The causes subdivide into the following four categories: 

A. Renal causes: Among these, the major categories are renal parenchymal disease (which includes chronic kidney disease and polycystic kidney disease) and reno-vascular disease (which includes renal artery stenosis and fibromuscular dysplasia).

B. Endocrine causes: Primary aldosteronism, Cushing syndrome/disease, hyperthyroidism, hypothyroidism, hyperparathyroidism, pheochromocytoma including drug-mediated pheochromocytoma crisis,[4] acromegaly, congenital adrenal hyperplasia.

C. Vascular: Coarctation of the aorta.

D. Other: Obstructive sleep apnea, drug-induced hypertension, pregnancy, scleroderma.

Drug-induced hypertension is a significant cause of secondary hypertension. Hence, it is essential to look at the patient's medication list. Following are the drugs that can cause hypertension[5]:

  • Non-steroidal anti-inflammatory drugs, acetaminophen, and aspirin are the commonest implicated drugs in the worsening of blood pressure control due to their widespread use
  • Sodium-containing antacids
  • Drugs used to treat attention-deficit/hyperactivity disorder(ADHD):  Methylphenidate, amphetamine, dexmethylphenidate, and dextroamphetamine
  • Anti-depressants: Monoamine oxidase inhibitors, tricyclic antidepressants, and serotonin-norepinephrine reuptake inhibitors
  • Atypical antipsychotics like clozapine and olanzapine
  • Decongestants that have phenylephrine or pseudoephedrine
  • Appetite suppressants
  • Herbal supplements like St John wort, ephedra, and yohimbine
  • Systemic corticosteroids like  dexamethasone, methylprednisolone, prednisone, prednisolone, and fludrocortisone
  • Mineralocorticoids like carbenoxolone, licorice, 9-alpha fludrocortisone and ketoconazole
  • Estrogens, androgens, and oral contraceptives
  • Immunosuppressants like cyclosporine
  • Chronic recombinant human erythropoietin
  • Recreational drugs: cocaine, methamphetamine, MDMA, bath salts
  • Nicotine, alcohol
  • Chemotherapeutic agents like gemcitabine (which causes microvascular injury)


As stated above, about 5 to 10% of hypertension in adults results from secondary hypertension. The prevalence of secondary hypertension varies with age, being most prevalent at the extremes of age, accounting for 70 to 85 percent of hypertension cases in children less than 12 years of age, and approximately 17 percent of cases in adults age 65 and older. The prevalence of secondary hypertension is lowest amongst hypertensive patients who are 19 to 39 years of age at 5 percent. The prevalence in adolescents (12 to 18 years) is 10 to 15%.[3]

History and Physical

Obtaining a complete history and performing a good physical exam is very important when trying to find the underlying cause of hypertension. The following history and physical exam findings point towards a specific cause of secondary hypertension:

  • Snoring, obesity, and daytime sleepiness could be indicative of obstructive sleep apnea.
  • History of renal insufficiency, atherosclerotic cardiovascular disease, edema may warrant further evaluation of chronic kidney disease (renal parenchymal disease).
  • History of recurrent urinary tract infections, kidney stones, acute/chronic abdominal/flank pain, hematuria, progressive renal failure may point towards autosomal dominant polycystic kidney disease (renal parenchymal disease).
  • A systolic/ diastolic abdominal bruit is audible in reno-vascular disease.
  • Use of sympathomimetics, acute stress, perioperative setting, tachycardia could all be in the context of excess catecholamines.
  • Decreased or delayed femoral pulses are seen in coarctation of the aorta.
  • Weight gain, fatigue, weakness, hirsutism, amenorrhea, moon facies, dorsal hump, purple striae, and truncal obesity present in Cushing syndrome/disease.
  • Paroxysmal hypertension, headaches, diaphoresis, palpitations, and tachycardia are features in pheochromocytoma.
  • Fatigue, weight loss, hair loss, diastolic hypertension, and muscle weakness are seen in hypothyroidism.
  • Heat intolerance, weight loss, palpitations, systolic hypertension, exophthalmos, tremor, and tachycardia will occur in hyperthyroidism.
  • Kidney stones, osteoporosis, depression, lethargy, and muscle weakness present in hyperparathyroidism.
  • Headaches, fatigue, visual problems, enlargement of the hands, feet, and tongue are features in acromegaly.
  • Heartburn, Raynaud phenomenon, nail pitting on the exam may be suggestive of scleroderma.


Laboratory tests and imaging modalities also help in diagnosing secondary hypertension. Some of the findings on common tests that can create suspicion for an underlying cause of hypertension are as follows: 

  • Basic Metabolic Panel (BMP): Hypokalemia presents in primary hyperaldosteronism and Cushing syndrome/disease. Also seen on the BMP in primary hyperaldosteronism, is metabolic alkalosis and hypernatremia. Blood urea nitrogen (BUN) and creatinine become elevated in renal parenchymal disease.
  • Complete blood count (CBC): Polycythemia can be present in obstructive sleep apnea.
  • Urine analysis: Proteinuria can be a feature in renal parenchymal disease.
  • Chest X-Ray in coarctation of aorta shows inferior rib notching and a figure of 3 sign (abnormality of the contour of the aorta).

Upon establishing suspicion for a particular cause based on history, physical exam findings, and common laboratory tests, certain tests can be used to specifically rule out or rule in a cause of secondary hypertension. They are as follows: 

  • Obstructive sleep apnea (OSA): Polysomnography (preferably in-laboratory polysomnography) is the diagnostic study of choice when there is a suspicion of obstructive sleep apnea. 
  • Primary hyperaldosteronism: A plasma aldosterone to renin ratio greater than 30, points towards a diagnosis of primary aldosteronism. A CT scan of the abdomen is also done to look for the presence of adenomas or hyperplasia of the adrenal glands.
  • Renal parenchymal disease: A decreased creatinine clearance occurs in renal parenchymal disease. Renal ultrasonography can be further used to determine the cause for the decreased creatinine clearance. Multiple cysts demonstrate in polycystic kidney disease, and a small contracted kidney is a feature in chronic kidney disease. Genetic testing can also be useful in ADPKD. 
  • Reno-vascular disease: Magnetic resonance angiography/CT angiography/doppler of renal arteries can all be used to look for the presence of stenosis of the renal arteries. Other tests that can be useful are captopril-augmented radioisotopic renography and renal arteriography.
  • Excess catecholamine use: If the patient is normotensive in the absence of high catecholamines, it rules out excess catecholamines as the cause.
  • Coarctation of the aorta: Doppler or CT imaging of the aorta will show a narrowing of the aorta. Echocardiography is another modality of choice.
  • Cushing syndrome/disease: Overnight 1 mg dexamethasone-suppression test and adrenocorticotropic hormone can help diagnose Cushing disease and syndrome.
  • Pheochromocytoma: Urinary catecholamine metabolites (vanillylmandelic acid, metanephrines, normetanephrines) become elevated in pheochromocytoma.
  • Hyper/hypothyroidism: Serum thyroid stimulating hormone, thyroxine, and triiodothyronine levels help diagnosing hyperthyroidism and hypothyroidism.
  • Hyperparathyroidism: Serum calcium and parathyroid hormone levels help in the diagnosis of hyperparathyroidism.
  • Acromegaly: Elevated growth hormone level can point towards acromegaly.
  • Scleroderma/ scleroderma renal crisis: Thrombotic microangiopathy, autoantibodies against RNA polymerase III, positive antinuclear antibody (ANA) will present in scleroderma. 

Treatment / Management

Management of secondary hypertension comprises of adequate control of blood pressure with antihypertensive drugs and addressing the secondary causes mentioned above. This section briefly discusses the management of the more common causes of secondary hypertension, viz: renal parenchymal disease, renovascular hypertension, primary hyperaldosteronism, obstructive sleep apnea, drug-induced hypertension, and pregnancy. 

A. Renal parenchymal disease:

Renal parenchymal disease-causing hypertension mainly involves chronic kidney disease (CKD) and autosomal dominant polycystic kidney disease (ADPKD).

i. Management of chronic kidney disease comprises of treating the reversible causes responsible for causing CKD (e.g., treating hypovolemia with fluids, avoid nephrotoxin use, relieve urinary tract obstruction) and slowing the rate of progression of the disease. To slow the rate of progression, adequate blood pressure control, decreasing urine protein, glycemic control, lifestyle changes like dietary protein restriction, and smoking cessation help. Angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs) are the best anti-hypertensives to use in proteinuric CKD. Bicarbonate use in patients with chronic metabolic acidosis slows progression to end-stage renal disease.[6]

ii. Patients with ADPKD eventually require renal replacement therapy. Before that stage reached, hypertension management is with anti-hypertensives: ACE inhibitors or ARBs and sodium restriction. Tolvaptan is an option in patients who are at high risk for progression to CKD. It decreases the rate of estimated glomerular filtration rate decline.[7] 

B. Renovascular hypertension:

Management of renovascular hypertension (i.e., renal artery stenosis from either atherosclerotic disease or fibromuscular dysplasia) divides into medical therapy and revascularization. Medical therapy involves the use of anti-hypertensives to control blood pressure and in the case of atherosclerotic disease, the use of antiplatelets, statins, diet, and lifestyle changes. ACE inhibitors and ARBs are the anti-hypertensives of choice. Other anti-hypertensives that are treatment options are calcium channel blockers and thiazide diuretics.

Revascularization is usually done by percutaneous angioplasty with stenting of the renal artery.  Surgery (which frequently includes aorto-renal bypass or sometimes removal of the ‘pressor’ kidney) is only for patients with complex anatomy.

In the following patients, revascularization may be more beneficial than medical therapy alone:

  • Patients with recurrent flash pulmonary edema
  • Failure or intolerance to optimal medical treatment
  • Refractory hypertension
  • Unexplained, progressive, a decline in renal function,
  • Recent initiation of dialysis in a patient with suspected renal artery stenosis
  • An acute increase in creatinine after medical therapy and in patients with a renal resistive index of less than 80 mmHg on Doppler

C. Primary hyperaldosteronism:

Unilateral primary hyperaldosteronism (e.g., unilateral adrenal hyperplasia or aldosterone-producing adenoma) gets treated with unilateral laparoscopic adrenalectomy. If the patient is not a surgical candidate or a patient has the bilateral adrenal disease, then medical management with a mineralocorticoid receptor antagonist is recommended- with spironolactone being the primary agent and eplerenone being the alternative.[8] 

D. Obstructive Sleep Apnea:

Continuous positive airway pressure (CPAP) therapy is the mainstay of treatment for OSA. To note, however, lifestyle modifications like weight loss, along with usage of CPAP have a synergistic effect on lowering blood pressure, and is better than either intervention alone.[9] 

An alternative to CPAP, are oral appliances, used in mild to moderate OSA, which are non-inferior to CPAP in the reduction of blood pressure and may even help with better compliance in patients. In patients refractory to the above treatment, few upper airway surgeries can be performed to help with symptoms and reduction in blood pressure, like uvulopalatopharyngoplasty (UPPP) in adults and tonsillectomy and adenoidectomy in children.  Along with these, anti-hypertensive drugs also help, particularly the ones that modulate the renin-angiotensin system (ACE inhibitors, ARBs, aldosterone antagonists, and beta blockers are the best options).[10]

E. Drug-induced hypertension: In drug-induced hypertension, upon identification of the culprit drug, the management is to withhold it and look for improvement.

F. Pregnancy: Hypertension in pregnancy comprises of chronic hypertension, gestational hypertension, pre-eclampsia, and eclampsia. Chronic hypertension is when hypertension occurs before pregnancy or before 20 weeks of gestation, whereas the other three occur after 20 weeks. Pre-eclampsia is associated with proteinuria, and eclampsia is associated with seizures.

Interventions for hypertension in pregnancy are lifestyle modifications and anti-hypertensives. The anti-hypertensives commonly used in pregnancy are labetalol, nifedipine, and methyldopa.

In cases of severe hypertension (severe preeclampsia, eclampsia, and HELLP syndrome), the standard of care is delivery, especially after 37 weeks of gestation. If an acute decrease in blood pressure is required, intravenous labetalol or intravenous hydralazine are options. Magnesium sulfate prevents seizures.[11][12]

Differential Diagnosis

The differential diagnosis of secondary hypertension as stated above are: chronic kidney disease, autosomal dominant polycystic kidney disease, renal artery stenosis, fibromuscular dysplasia, primary aldosteronism, Cushing syndrome/disease,  hyperthyroidism, hypothyroidism, hyperparathyroidism, pheochromocytoma, acromegaly, congenital adrenal hyperplasia, coarctation of aorta, obstructive sleep apnea, drug-induced hypertension, pregnancy, scleroderma.


The prognosis of secondary hypertension is good. With the treatment of the underlying condition, the blood pressure may decrease or even come back to normal.


The underlying medical condition that causes high blood pressure can be worsened by secondary hypertension. Some of the complications of secondary hypertension are atherosclerosis, aneurysm, heart failure, metabolic syndrome, chronic renal failure, and retinopathy.[13]


  • Internal medicine
  • Nephrology
  • Cardiology
  • Endocrinology
  • Vascular surgery

Enhancing Healthcare Team Outcomes

The patient's primary care doctor and/or nurse practitioner may be the main person involved in diagnosing a secondary cause of hypertension. But an interprofessional team of specialists consisting of a nephrologist, cardiologist, endocrinologist, rheumatologist, and surgeons can help with diagnosing and managing the patient. Nurses also play an essential role in patient care, as do pharmacists. Hence, interprofessional communication and care coordination between physicians, nurses, and other health professionals are crucial to enhance patient outcomes. [Level V]

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Secondary Hypertension - Questions

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A 22-year-old woman presents to a routine well-woman visit. She has never had a pap smear and desires to do so today. Having completed the initial screen, the nurse reports that the patient's blood pressure was 150/90 mmHg. The remainder of her vital signs, including BMI, are within normal limits. The patient has no significant past medical history and no prior surgeries. Her family history is similarly unremarkable. Her father was diagnosed at age 45 with hypertension and suffered a myocardial infarction at the age of 50. The patient's current medication's include norethindrone-ethinyl estradiol oral contraceptive pill, extended release mixed amphetamine salts 20 mg every morning with breakfast, immediate release mixed amphetamine salts 10 mg every afternoon shortly after lunch, topical clindamycin-benzoyl peroxide gel, fluticasone nasal spray, cetirizine, pseudoephedrine as needed, and ibuprofen 800mg as needed. The patient states she is very anxious about the pap smear. A 24-hour ambulatory blood pressure monitor is performed to rule out "white coat hypertension", and the results confirm this patient has consistently elevated blood pressure at home as well. What is the next step in the evaluation and/or treatment of this patient?

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Aa 28-year-old male has a past medical history significant for obstructive sleep apnea and recently diagnosed essential hypertension. One week ago a colleague in your office started this patient on chlorthalidone 12.5 mg daily and asked him to return in 7 days to see how things were going on the new medication. The patient also had a basic metabolic panel (BMP) drawn the day of the prior appointment and a repeat BMP yesterday morning. Today the patient is afebrile, and the remainder of his vitals are as follows: heart rate of 88 beats/min, blood pressure 154/92 mmHg, and respiratory rate 14. Generally, he feels well today but does note that he feels like he has been a little weak at the gym the past couple of days, and he had bad cramps yesterday after his workout. While reviewing his BMP, you note that his potassium dropped from 3.6 mEq/L 1 week ago to 3.3 mEq/L the day before the appointment. Which of the following is the most appropriate next step?

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A 34-year-old woman with a past medical history of systemic lupus erythematosus on chronic steroids and recently diagnosed Raynaud phenomenon presents to the hospital with a severe throbbing headache and blurring of vision. Vital signs show a blood pressure of 210/120 mmHg. On examination, she is noted to have some digital nail pitting and bilateral papilledema. No abdominal bruit is present. Laboratory values are significant for thrombocytopenia, normocytic anemia, increased indirect bilirubin, decreased haptoglobin, elevated LDH, BUN 23 mg/dl, serum creatinine 3 mg/dl, and glucose 112 mg/dl. Urine analysis shows mild proteinuria. The patient has no known kidney disease, no history of hypertension, and laboratory values from 6 months ago were all within normal limits. On further questioning about her past medical history, she states that she had some recent onset of heartburn for which she has been taking omeprazole. Which of the following is the most likely cause for her sudden increase in blood pressure?

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A 45-year-old male presents to the clinic complaining of a high blood pressure, which was an incidental finding during a routine health check at his workplace. He has had no previous episodes of hypertension and has no other past medical history. He complains of occasional episodes of flank pain. Family history is significant for renal failure requiring dialysis in his mother and hypertension in his brother. Current blood pressure is 160/110 mmHg. Other vitals are within normal limits, and physical exam shows bilateral flank fullness. Complete blood count and basic metabolic panel are within normal limits. Urine analysis shows proteinuria and hematuria. Which of the following is the next best step in the management of this patient?

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A 35-year-old woman with a history of schizophrenia and depression presents to the clinic for a routine 3-month follow-up. She takes olanzapine for her schizophrenia and St. John's Wort and escitalopram for her depression, all of which she started taking a few months ago. She is sexually active and is on oral contraceptive pills (OCPs). Her other medication is ibuprofen, which she takes occasionally for back pain. She has no complaints. On examination, her blood pressure is noted to be 146/90 mmHg, which was 120/80 mmHg during her visit three months ago. Which of the following best identifies the medications that can contribute to her blood pressure?

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A 65-year-old male is admitted to the hospital for evaluation of chest discomfort. The patient has a history of uncontrolled hypertension and is on multiple antihypertensive medications. This is his 2nd admission in the past 3 months. He is a smoker and drinks alcohol occasionally. He also reports excessive daytime sleepiness and generalized fatigue for the past few months. On examination, the patient appears to be in mild distress. Vital signs reveal a heart rate of 84 beats per minute, blood pressure of 188/96 mm Hg, respiratory rate of 26 breaths per minute, oxygen saturation of 96% on 2 liters nasal cannula, and a BMI of 42 kg/m2. The remainder of the examination is unremarkable. Lab tests reveal a Hemoglobin of 16 mg/dL and WBC of 6.7 mg/dL. The basic chemistry profile is within normal limits. Troponin T is 0.010 and ProBNP is 42. His EKG appears similar to previous baseline EKG, with no new changes. A chest x-ray is also done which appears unremarkable. Which of the following is the most appropriate test to diagnose this patient’s persistent hypertension?

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Secondary Hypertension - References


Charles L,Triscott J,Dobbs B, Secondary Hypertension: Discovering the Underlying Cause. American family physician. 2017 Oct 1;     [PubMed]
Rimoldi SF,Scherrer U,Messerli FH, Secondary arterial hypertension: when, who, and how to screen? European heart journal. 2014 May 14;     [PubMed]
Viera AJ,Neutze DM, Diagnosis of secondary hypertension: an age-based approach. American family physician. 2010 Dec 15;     [PubMed]
Aronow WS, Drug-induced causes of secondary hypertension. Annals of translational medicine. 2017 Sep;     [PubMed]
Drawz PE,Rosenberg ME, Slowing progression of chronic kidney disease. Kidney international supplements. 2013 Dec;     [PubMed]
Chebib FT,Perrone RD,Chapman AB,Dahl NK,Harris PC,Mrug M,Mustafa RA,Rastogi A,Watnick T,Yu ASL,Torres VE, A Practical Guide for Treatment of Rapidly Progressive ADPKD with Tolvaptan. Journal of the American Society of Nephrology : JASN. 2018 Oct;     [PubMed]
Funder JW,Carey RM,Mantero F,Murad MH,Reincke M,Shibata H,Stowasser M,Young WF Jr, The Management of Primary Aldosteronism: Case Detection, Diagnosis, and Treatment: An Endocrine Society Clinical Practice Guideline. The Journal of clinical endocrinology and metabolism. 2016 May;     [PubMed]
Chirinos JA,Gurubhagavatula I,Teff K,Rader DJ,Wadden TA,Townsend R,Foster GD,Maislin G,Saif H,Broderick P,Chittams J,Hanlon AL,Pack AI, CPAP, weight loss, or both for obstructive sleep apnea. The New England journal of medicine. 2014 Jun 12;     [PubMed]
Ahmad M,Makati D,Akbar S, Review of and Updates on Hypertension in Obstructive Sleep Apnea. International journal of hypertension. 2017;     [PubMed]
ACOG Practice Bulletin No. 203: Chronic Hypertension in Pregnancy. Obstetrics and gynecology. 2019 Jan;     [PubMed]
Kattah AG,Garovic VD, The management of hypertension in pregnancy. Advances in chronic kidney disease. 2013 May;     [PubMed]
Hosseinnezhad A,Black RM,Aeddula NR,Adhikari D,Trivedi N, Glucagon-induced pheochromocytoma crisis. Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists. 2011 May-Jun     [PubMed]
Vaidya SR,Aeddula NR, Chronic Renal Failure . 2019 Jan     [PubMed]


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