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The malignant phase of hypertension (malignant nephrosclerosis)

Malignant nephrosclerosis is a kidney disease associated with a malignant or accelerated phase of hypertension. Hypertension of this type usually develops in previously normotensive patients, and also often in patients who have previously experienced essential benign hypertension, secondary forms of hypertension, or chronic renal disease, especially glomerulonephritis and reflux nephropathy. It is also a common cause of uremia and death of patients with scleroderma. Malignant hypertension is a relatively rare disease, observed only in 1-5% of all individuals with high blood pressure, usually affects younger people, characterized by a higher predisposition to men.

Malignant hypertension is associated with high levels of renin, angiotensin, and aldosterone. Any stimulus that causes hyperreninemia leads to vasospasm and an increase in blood pressure, followed by necrosis of the vessels of the kidneys and other organs. This increase in blood pressure causes endothelial damage, thrombosis, fibrinoid necrosis, and intravascular coagulation. With malignant hypertension using ischemia, a vicious cycle of hyperreninemia is included. An increase in the content of other vasoconstrictors (e.g. endothelin) or a decrease in the concentration of vasodilators (e.g. nitric oxide) causes spasm and vascular damage. Any mechanism of malignant hypertension leads to renal failure due to renal ischemia due to narrowing of arteries and arterioles.

The size of the kidneys depends on the predisposition to the disease and the severity of hypertension.
Small petechial hemorrhages, in the form of flea bites, occur on the cortical surface of the kidneys and are associated with ruptures of the arterioles or glomerular capillaries. In malignant hypertension, two types of damage to blood vessels are described:

• fibrinoid necrosis of arterioles, manifested in the form of eosinophilic granular changes in the wall of blood vessels, which are stained with fibrin. In addition, inflammatory infiltrate is often found in the vascular wall, indicating the development of necrotizing arteriolitis;

• thickening of intima in the interlobular arteries and arterioles caused by the proliferation of elongated, concentrically located cells and smooth muscle cells simultaneously with the appearance of thin layers of concentrically located collagen fibers. These changes are called concentric arteriolitis, as well as bulbous arteriolitis. They correlate well with renal failure in malignant hypertension. Sometimes the glomeruli are necrotic and infiltrated by neutrophils, the glomerular capillaries are thrombosed (necrotizing glomerulonephritis) (Fig. 18.17). Damage to arteries and arterioles leads to malignant narrowing of the lumen of the vessels with ischemic atrophy and heart attack, developing distal to the affected vessels.

Fig. I8. 17.

Malignant nephrosclerosis


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The malignant phase of hypertension (malignant nephrosclerosis)

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