Secondary Hypertension
Increased blood pressure (BP), which is secondary to an underlying cause. About 5 to 10% of cases are due to secondary hypertension.
Clinical clues suggesting secondary hypertension:
- Resistant hypertension
- Sudden rise in blood pressure in a patient who had previously stable pressures.
- Patients with severe hypertension and patients with end-organ damage like acute kidney injury, neurological manifestations, flash pulmonary edema, hypertensive retinopathy.
- Associated with hypokalemia or metabolic alkalosis.
- Onset of hypertension before puberty.
- Non-dipping or reverse dipping in blood pressure occurs while monitoring 24-hour ambulatory blood pressure.
Causes:
The causes of secondary hypertension include:
- Renal causes: Renal parenchymal disease and renovascular disease.
- Endocrine causes: Primary aldosteronism, Cushing syndrome or disease, hyperthyroidism, hyperparathyroidism, pheochromocytoma.
- Vascular: Coarctation of the aorta
- Other: Drug-induced hypertension, Obstructive sleep apnea, pregnancy
Diagnosis:
Specific Investigations according to clinical conditions are:
- Reno-vascular disease: Magnetic resonance angiography, CT angiography, or color doppler.
- Obstructive sleep apnea (OSA): Polysomnography
- Primary hyperaldosteronism: Plasma aldosterone to renin ratio greater than 30 indicates the presence of primary hyperaldosteronism. A CT scan of the abdomen is performed to detect adenomas or adrenal hyperplasia.
- Renal parenchymal disease: In renal parenchymal disease, creatinine clearance is reduced. Renal ultrasonography can be used to further investigate the cause of the decreased creatinine clearance.
- Coarctation of the aorta: Doppler or CT scan of the aorta will reveal narrowing of the aorta.
- Cushing syndrome/disease: A 1 mg dexamethasone suppression test performed overnight, and adrenocorticotropic hormone test can aid in the diagnosis of the disease.
- Pheochromocytoma: Urinary catecholamine metabolites such as vanillylmandelic acid, metanephrines, normetanephrines become elevated in pheochromocytoma.
- Hyper or hypothyroidism: Serum thyroid stimulating hormone, thyroxine, and triiodothyronine levels help diagnosing hyperthyroidism and hypothyroidism.
Treatment:
Secondary hypertension management involves controlling blood pressure with antihypertensive medications and addressing secondary causes.
A. Renal parenchymal disease:
Renal parenchymal disease causing hypertension mainly involves chronic kidney disease (CKD) and autosomal dominant polycystic kidney disease (ADPKD).
- i. Chronic kidney disease management consists of treating the reversible causes of CKD (e.g., treating hypovolemia with fluids, avoiding nephrotoxin use, relieving urinary tract obstruction) and slowing the disease's progression. Adequate control of blood pressure, decreasing urinary protein, glycemic control, lifestyle changes such as dietary protein restriction, and smoking cessation help to slow the rate of progression.
In proteinuric CKD, the best antihypertensives to use are angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs). Bicarbonate treatment slows the progression to end-stage renal disease in patients with chronic metabolic acidosis. - ii. Patients suffering from ADPKD will eventually require renal replacement therapy. Before that point, hypertension is managed with antihypertensives such as ACE inhibitors or ARBs and also sodium restriction. Tolvaptan is an option for patients who are at high risk of progression to CKD. It slows the rate of decline in estimated glomerular filtration rate.
B. Renovascular hypertension:
Renovascular hypertension(renal artery stenosis caused by atherosclerotic disease or fibromuscular dysplasia) is managed with medical therapy and revascularization. Antihypertensives are used to control blood pressure, and in the case of atherosclerotic disease, antiplatelets, statins, diet, and lifestyle changes are used.
Percutaneous angioplasty with renal artery stenting is the most common method of revascularization. Revascularization may be beneficial than medical therapy alone in patients with refractory hypertension, flash pulmonary edema, progressive decrease in renal function.
C. Primary hyperaldosteronism:
Unilateral primary hyperaldosteronism(e.g., aldosterone producing adenoma or unilateral adrenal hyperplasia) is treated with unilateral laparoscopic adrenalectomy. If the person is not a candidate for surgery or has bilateral adrenal disease, medical management with a mineralocorticoid receptor antagonist—spironolactone as the primary agent and eplerenone as an alternative—is recommended.
D. Obstructive Sleep Apnea:
Continuous positive airway pressure therapy is the cornerstone of OSA treatment. However, lifestyle changes such as weight loss combined with CPAP have a synergistic effect on lowering blood pressure and are superior to either intervention alone.
E. Drug-induced hypertension:
When the culprit drug is identified in drug-induced hypertension, the management is to withhold it and wait for improvement.
F. Pregnancy:
Chronic hypertension, gestational hypertension, pre-eclampsia, and eclampsia are different forms of hypertension in pregnancy. Chronic hypertension indicates you had high blood pressure before pregnancy or before 20 weeks of gestation, whereas the other three occur after 20 weeks of gestation. Proteinuria is associated with pre-eclampsia, and seizures are associated with eclampsia.
Lifestyle changes and antihypertensives are two interventions for hypertension in pregnancy. Labetalol, nifedipine, and methyldopa are common antihypertensives used during pregnancy.
