Renal hypertension
Renal pathology is historically and clinically the most significant cause of secondary blood pressure elevation. Three broad groups of diseases lead to this condition:
- Renoparenchymal diseases. In this case, blood pressure rises steadily due to diffuse or focal damage to the functional kidney tissue itself (parenchyma). This category includes chronic glomerulonephritis, pyelonephritis, severe diabetic glomerulosclerosis, and interstitial nephritis. In addition, the parenchyma is severely affected by systemic amyloidosis, renal tuberculosis, various rheumatic diseases, and specific nephropathy of pregnancy. Malignant neoplasms occupy a distinct oncological niche: hypernephroid carcinoma and nephroblastoma (known as Wilms tumor).
- Renovascular diseases. Here, the problem lies exclusively in 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. Sometimes the vessel is mechanically compressed from the outside by pathological processes.
- Renal developmental anomalies. Congenital anatomical defects also consistently lead to severe hemodynamic shifts. These include aplastic and hypoplastic kidney, marked polycystic kidney disease, dystopia (atypical location), as well as hydronephrosis and megaureter.
Endocrine hypertension
Hormonal imbalance has a profound effect on vascular tone, cardiac function, and total circulating blood volume. The classification is based on the affected gland:
- Adrenal forms. Occur due to excessive uncontrolled hormone secretion by the adrenal cortex or medulla. Typical clinical examples include primary aldosteronism, hormone-secreting pheochromocytoma, Cushing's disease and syndrome, and various adrenocortical adenomas.
- Pituitary forms. Directly related to pathological hypersecretion of pituitary tropic hormones. This is clearly manifested in acromegaly or specific ACTH-dependent forms of hypertension.
- Thyroid and parathyroid forms. Persistent blood pressure elevation is observed against the background of hyperthyroidism and hyperparathyroidism.
- Other endocrine factors. This group traditionally includes climacteric hypertension, which develops against the background of age-related bodily changes, as well as carcinoid syndrome.
Cardiovascular and other forms
Hemodynamic (or cardiovascular) hypertension is caused by gross mechanical obstacles to normal blood flow or changes in the rheological properties of the blood itself.
- Aortic pathology. Congenital coarctation of the aorta, pronounced systemic atherosclerosis, or aortic valve regurgitation creates abnormal pressure distribution in the vascular bed.
- Systemic hemodynamic disorders. This subgroup includes congestive circulatory failure, complete atrioventricular block, various heart defects, and essential hyperkinetic syndrome.
- Changes in blood composition. A striking hematological example is polycythemia vera (erythemia). In this disease, blood viscosity increases, which forces the heart to work with an increased load.
- Neurogenic hypertension. A persistent increase in pressure is provoked by organic brain diseases or severe polyneuropathies.
- Medication triggers. Iatrogenic hypertension can develop rapidly due to the use of glucocorticoids, mineralocorticoids, oral contraceptives, and certain other drugs.
- Specific conditions. These include gestational hypertension (geSToz), as well as isolated hypertension of individual organs (for example, pulmonary hypertension or portal hypertension).
Briefly: answers to topical questions
Which heart defects lead to the development of 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 increased systolic pressure.
- Aortic valve regurgitation — blood regurgitation into the left ventricle during diastole, which increases the load on it and raises blood pressure.
Unspecified heart defects accompanied by hemodynamic disorders are also mentioned in the 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 arteriolitis — intimal thickening due to smooth muscle cell proliferation and concentric arrangement of collagen fibers around a sharply narrowed lumen.
- Fibrinoid necrosis — segmental necrosis of the walls of afferent arterioles and glomerular capillaries.
- Aneurysm formation — formation of outpouchings in the walls of affected arterioles.
- Thrombosis — thrombosis of capillaries against the background of necrotizing glomerulonephritis.
For quick memorization of the main groups of secondary hypertension, use the acronym PEK-N: Penal, Endocrine, Cardiovascular, Neurogenic.
Class and exam questions
How does symptomatic hypertension differ from essential hypertension?
In symptomatic hypertension, high blood pressure is a consequence of a specific disease (e.g., an adrenal tumor or renal artery stenosis). In hypertension (essential), the elevation of blood pressure 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 divided into parenchymal, vascular, and developmental anomalies.
What endocrine adrenal pathologies cause blood pressure elevation?
These include pheochromocytoma, primary aldosteronism, adrenocortical adenoma, as well as Cushing's disease and syndrome.
What else to study on this topic
- Pathogenesis of renovascular hypertension and the role of the renin-angiotensin system.
- Morphological changes in the kidneys in diabetic glomerulosclerosis.
- Mechanisms of hypertension development in pheochromocytoma and carcinoid syndrome.
- Hemodynamics in coarctation of the aorta and aortic valve regurgitation.
- Clinical features and complications of gestational hypertension.
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