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Malignant phase of hypertension (malignant nephrosclerosis)



Malignant nephrosclerosis is a kidney disease associated with the malignant or accelerated phase of hypertension. Hypertension of this type usually develops in previously normotensive patients, and also often in patients who have previously suffered from essential benign hypertension, secondary forms of hypertension or chronic renal diseases, especially glomerulonephritis and reflux nephropathy. It is also a common cause of uraemia and death of patients with scleroderma. Malignant hypertension is a relatively rare disease, it is observed only in 1–5% of all individuals with high blood pressure, usually affects younger people, and is characterized by a higher predisposition to it for 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. Such an increase in blood pressure causes endothelial damage, thrombosis, fibrinoid necrosis and intravascular coagulation. For malignant hypertension with ischemia, the vicious cycle of hyperreninemia is included. An increase in the content of other vasoconstrictors (for example, endothelin) or a decrease in the concentration of vasodilators (for example, nitric oxide) causes spasm and vascular damage. Any mechanism of malignant hypertension leads to renal failure due to renal ischemia due to narrowing of the arteries and arterioles.

The size of the kidneys depends on the susceptibility to the disease and the severity of hypertension.
Small petechial hemorrhages, having the appearance of flea bites, are found on the cortical surface of the kidneys and are associated with ruptures of the arterioles or capillaries of the glomeruli. For malignant hypertension, two types of damage to the blood vessels are described:

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

• intimal thickening 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 arranged collagen fibers. These changes are called concentric arteriolitis, as well as bulbous arteriolitis. They correlate well with renal insufficiency in malignant hypertension. Sometimes the glomeruli are necrotized and infiltrated with neutrophils, the capillaries of the glomeruli are thrombosed (necrotizing glomerulonephritis) (Fig. 18.17). Damage to the arteries and arterioles leads to a 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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Malignant phase of hypertension (malignant nephrosclerosis)

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