Secondary (symptomatic) arterial hypertension refers to a diverse group of pathological conditions in which a sustained elevation in blood pressure is not an independent disease, but a clinical sign of an underlying primary disorder. Unlike essential hypertension, a specific primary pathology affecting a particular organ or system can always be identified.
PrevalenceAccounts for 5–6% of all patients with elevated blood pressure.
Renal CausesRepresent 12–15% of all diagnosed types of hypertension.
Endocrine CausesUnderlie 2–3% of cases of arterial hypertension.
Cardiovascular CausesAccount for approximately 2% of blood pressure elevation cases.
Renal Hypertension
Renal pathology is historically and clinically the most significant cause of secondary blood pressure elevation. Three broad categories of renal disease lead to this condition:
Renoparenchymal diseases. In this case, blood pressure rises steadily due to diffuse or focal damage to the renal parenchyma itself. This category includes chronic glomerulonephritis, pyelonephritis, severe diabetic glomerulosclerosis, and interstitial nephritis. Additionally, the parenchyma is significantly affected by systemic amyloidosis, renal tuberculosis, various rheumatic diseases, and specific nephropathy of pregnancy. Malignant neoplasms occupy a distinct oncological niche: renal cell carcinoma and nephroblastoma (known as Wilms tumor).
Renovascular diseases. Here, the problem stems strictly from impaired main blood flow through the renal arteries. The lumen of a large vessel can become critically narrowed due to atherosclerotic stenosis or fibromuscular dysplasia. Acute disruption of blood supply occurs when the artery is occluded by a thrombus or embolus. Occasionally, the vessel is mechanically compressed from the outside by pathological processes.
Congenital renal anomalies. Congenital anatomical defects also predictably lead to severe hemodynamic shifts. These include aplastic and hypoplastic kidneys, marked polycystic kidney disease, dystopia (abnormal anatomical location), as well as hydronephrosis and megaureter.
Endocrine Hypertension
Hormonal imbalances exert a powerful influence on vascular tone, cardiac function, and total circulating blood volume. Classification is based on the affected gland:
Adrenal forms. These occur with excessive, uncontrolled hormone secretion by the adrenal cortex or medulla. Typical clinical examples include primary aldosteronism, hormonally active pheochromocytoma, Cushing's disease and syndrome, and various adrenocortical adenomas.
Pituitary forms. Directly linked to pathological hypersecretion of trophic pituitary hormones. This is prominently manifested in acromegaly or specific ACTH-dependent forms of hypertension.
Thyroid and parathyroid forms. Sustained blood pressure elevation is observed against the background of hyperthyroidism and hyperparathyroidism.
Other endocrine factors. This group traditionally includes menopausal hypertension, which arises from age-related bodily restructuring, as well as carcinoid syndrome.
Cardiovascular and Other Forms
Hemodynamic (or cardiovascular) hypertension is caused by gross mechanical obstacles to normal blood flow or alterations in the rheological properties of the blood itself.
Aortic pathology. Congenital coarctation of the aorta, pronounced systemic atherosclerosis, or aortic valve regurgitation creates an abnormal pressure distribution within the vascular bed.
Systemic hemodynamic disturbances. This subcategory includes congestive heart failure, complete atrioventricular block, various valvular heart defects, and essential hyperkinetic syndrome.
Alterations in blood composition. Polycythemia vera is a prominent hematologic example. In this condition, blood viscosity increases, forcing the heart to work against an increased workload.
Neurogenic hypertension. A sustained elevation in blood pressure is triggered by organic brain diseases or severe polyneuropathies.
Drug-induced triggers. Iatrogenic hypertension can develop rapidly due to the use of glucocorticoids, mineralocorticoids, oral contraceptives, and certain other medications.
Specific conditions. These include preeclampsia in pregnancy, as well as isolated hypertension of specific organs (e.g., pulmonary hypertension or portal hypertension).
Mnemonic
To quickly memorize the main groups of secondary hypertension, use the mnemonic PEN-C: Pararenal/Renal, Endocrine, Neurogenic, Cardiovascular.
Frequently asked questions
Which heart defects lead to hemodynamic arterial hypertension?
Hemodynamic (cardiovascular) arterial hypertension is caused by the following aortic and valvular defects:
Coarctation of the aorta — a congenital narrowing of the vessel distal to the left subclavian artery, causing impaired blood flow and elevated systolic pressure.
Aortic valve regurgitation — backflow of blood into the left ventricle during diastole, which increases ventricular preload and raises blood pressure.
Unspecified heart defects accompanied by hemodynamic disturbances are also cited in sources.
Which organic brain diseases cause neurogenic arterial hypertension?
Neurogenic (centrogenic and cerebroischemic) arterial hypertension is caused by the following organic lesions of brain structures:
Ischemia — impaired cerebral blood supply due to atherosclerosis or vascular thrombosis (ischemia of the medulla oblongata is particularly critical).
Hemorrhage — localized damage to brain structures.
Brain tumors — lead to compression of brain tissue.
Encephalitis — an inflammatory disease causing localized damage to brain structures.
What microscopic changes develop in renal arterioles in malignant arterial hypertension?
In malignant arterial hypertension, the following microscopic changes develop in renal arterioles:
Concentric arteriolosclerosis — thickening of the intima due to smooth muscle cell proliferation and concentric deposition of collagen fibers around a sharply narrowed lumen.
Fibrinoid necrosis — segmental necrosis of the walls of afferent arterioles and glomerular capillaries.
Aneurysm formation — development of outpouchings in the walls of affected arterioles.
Thrombosis — thrombosis of capillaries associated with necrotizing glomerulonephritis.
How does secondary hypertension differ from essential hypertension?
In secondary hypertension, high blood pressure is a consequence of a specific underlying disease (such as an adrenal tumor or arterial stenosis). In essential hypertension, blood pressure elevation is an independent primary pathology.
Which group of secondary hypertension is most common?
Renal hypertension. It accounts for 12–15% of all cases of elevated blood pressure and is subdivided into parenchymal, vascular, and congenital anomaly types.
What endocrine adrenal pathologies cause blood pressure elevation?
These include pheochromocytoma, primary aldosteronism, adrenocortical adenoma, and Cushing's disease and syndrome.
Go deeper
Pathogenesis of renovascular hypertension and the role of the renin-angiotensin-aldosterone system.
Morphological changes in the kidneys in diabetic glomerulosclerosis.
Mechanisms of hypertension in pheochromocytoma and carcinoid syndrome.
Hemodynamics in aortic coarctation and aortic valve regurgitation.
Clinical course and complications of preeclampsia in pregnancy.