Malignant arteriole kidney caused by primary malignant hypertension in the elderly

Introduction of malignant arterioles and kidneys caused by primary malignant hypertension in the elderly If a patient's many years of benign hypertension or renal parenchymal hypertension is converted to malignant hypertension (rapid type) or a disease in a few weeks or months, it is characterized by acute hypertension, which often causes severe renal pathological changes. Malignant nephrosclerosis. Renal function rapidly declines and progressive renal failure occurs. basic knowledge The proportion of illness: 0.0005% Susceptible people: the elderly Mode of infection: non-infectious Complications: acute left heart failure in the elderly, hypertensive encephalopathy, renal failure

Malignant arteriolar nephropathy caused by primary malignant hypertension in the elderly

(1) Causes of the disease

Malignant arteriolar atherosclerosis is caused by acute or malignant hypertension. At this time, the arterial lesions were mainly fibrinous necrosis of the arterial wall and thickening of the endometrium.

1. Cellulose-like necrosis This lesion is considered to be a characteristic lesion of malignant hypertension, except in the arcuate artery, interlobular artery, and small arteriole, and can extend from the small artery to the glomerular capillaries. Hey. The occurrence of fibrinoid necrosis is related to severe hypertension itself. It has been found that the diastolic blood pressure needs to be as high as 150mmHg before the small arterial wall necrosis occurs, and the higher necrosis is more serious; and it is related to many vasoactive substances abnormalities at this time, including renin- Angiotensin-aldosterone (RAS) is over-activated, vasopressin activity is enhanced, prostacyclin is decreased, and kinin levels are decreased. In addition, fibrinoid necrosis may also cause local coagulation and intracellular calcium with vascular endothelial injury. Factors such as increased content.

2. Intimal thickening is similar to benign small arteriosclerosis, and mainly affects the interlobular artery and the arcuate artery wall. The pathogenesis is the same as that of benign small arteriosclerosis.

(two) pathogenesis

The size of the kidney can be normal (such as secondary hypertension caused by chronic renal parenchymal disease, the kidneys can be reduced). The kidney surface can have a bit of bleeding like a bite. There are two characteristic pathological changes seen under the microscope:

1 cellulose-like necrosis of the small arteries;

2 proliferative endarteritis of the interlobular artery, the former is considered to be a pathological feature of malignant small arteriosclerosis, which is characterized by the deposition of granular cellulose-like substance in the middle layer of the small arterial wall, or deposited in the inner membrane, eosin Hematoxylin staining was bright pink, Masson stained dark red, and histochemical and immunofluorescence techniques confirmed fibrin; the middle layer of muscle fibers no longer existed, the nucleus disappeared or only fragments were left; red blood cells or fragments thereof infiltrated into small arteries The flap causes punctiform hemorrhage on the surface of the kidney; the lumen is narrowed due to thickening of the wall and fibrin thrombosis in the blood vessel; sometimes polymorphonuclear leukocytes and monocytes also infiltrate the vessel wall and present as necrotizing arteriitis. Proliferative endarteritis manifests as a thickening of the intima leading to a moderate to high stenosis of the lumen. In severe cases, the inner diameter is only a single red blood cell size, and occasionally it can be completely occluded by fibrin plugs. There are three types of thickened intima: onion skin type: surrounded by elongated endometrial cells and concentric layers of connective tissue fibrils, the middle layer is stretched outward.

Malignant small artery renal prevention caused by primary malignant hypertension in the elderly

The risk factors for this disease are as follows:

Cellulose-like necrosis and proliferative endarteritis of the small arteries of this disease are directly caused by the mechanical stress of the blood vessel wall caused by severe hypertension. Although the malignant state of hypertension causes different causes, it has severe hypertension. If it can effectively control blood pressure, the malignant state can also be reversed. Sympathectomy was performed from patients with severe hypertension, and renal biopsy was performed at the same time. It was found that small arterial necrosis occurred only when the general diastolic blood pressure reached 20 kPa (150 mmHg). If it is higher, necrosis is more serious. In patients with one-sided renal artery stenosis secondary to malignant hypertension, renal artery necrosis occurs only in the contralateral kidney, and the stenosis side does not occur. Animal experiments have clearly shown that severe hypertension can cause pathological changes similar to human malignant small arteriosclerosis.

The main point of vascular poisoning on the above stress theory is that there is a lot of overlap between the blood pressure of patients with benign hypertension and malignant hypertension. Even some patients have persistent severe hypertension for a long time, but they are not. In a malignant state, some scholars have suggested that a sudden change from a severe benign hypertension with few symptoms to a malignant hypertension with obvious symptoms and multiple systemic damage may involve other factors in addition to hypertension. Vascular poisoning is one of them.

Malignant small artery and renal complications caused by primary malignant hypertension in the elderly Complications, elderly acute left heart failure, hypertensive encephalopathy, renal failure

Often complicated by acute left heart failure and hypertensive encephalopathy, renal failure and so on.

Malignant small arterial kidney symptoms caused by primary malignant hypertension in the elderly Common symptoms Fatigue polyuria abdominal pain Nocturia increased dyspnea less urinary hematuria Proteinuria hemianopia ESR increased

The onset is usually very urgent (often remember the exact date), the most common symptoms are headache, blurred vision and weight loss, followed by difficulty breathing, fatigue, discomfort, nausea, vomiting, upper abdominal pain, polyuria, nocturia and the naked eye. hematuria. Headache symptoms are not specific, but severe hypertension with newly developed headaches or transition to persistence should be carefully considered to turn to malignant. 76% of newly diagnosed patients have visual symptoms, and 90% will always occur. The most common of these are blurred vision and decreased vision, 14% of sudden blindness, and blind spots, diplopia and hemianopia. Weight loss is another early symptom, the cause of which is (at least in part) due to the natural diuretic and decreased blood volume at the onset of the malignant state (see above), and often occurs before anorexia and uremia. The blood pressure is obviously elevated, and the diastolic blood pressure is generally more than 16.0 to 17.3 kPa (120-130 mmHg). Because of the considerable overlap of blood pressure values between benign hypertension and malignant hypertension, there is no specific critical blood pressure for malignant hypertension. Height, such as the original normal blood pressure, such as diastolic blood pressure rose to 13.3 ~ 14.7kPa (100 ~ 110mmHg), may be malignant. On the contrary, there are also people with essential hypertension who have very high diastolic blood pressure and continue for many years, and have not entered a malignant state.

The damage of blood vessels caused by malignant hypertension is systemic progressive vascular disease, and the time involved in the kidney is relatively late (this is malignant small arteriosclerosis), and its clinical manifestations can be from a small amount of proteinuria without renal dysfunction to severe kidney. Functional failure, which sometimes cannot even be distinguished from end-stage primary renal parenchymal disease. Can be roughly divided into 4 types:

1 subacute progression (weeks to months) until end-stage renal failure (death within 1 year), seen in cases of inadequate treatment.

2 only temporary renal damage, seen in the early stage of the disease can effectively control blood pressure.

3 Hypertensive neuroretinopathy (see below), severe hypertension, and renal failure have been found in malignant hypertension.

4 oliguric acute renal failure.

Examination of malignant arterioles and kidneys caused by primary malignant hypertension in the elderly

Laboratory examination: blood routine red blood cells and hemoglobin are generally no abnormalities, but acute hypertensive patients may have Coombs test negative microvascular hemolytic anemia, with red blood cells, high hemoglobin increased blood viscosity, prone to thrombosis complications (including brain Infarction) and left ventricular hypertrophy.

Urine routine: Early patients have normal urine routine, and the urine specific gravity is gradually reduced when the renal concentrating function is impaired. There may be a small amount of urinary protein, red blood cells, and occasional casts. As the renal lesion progresses, the amount of urinary protein increases. In patients with benign renal cirrhosis, such as 24h urine protein above 1g, the prognosis is poor. Red blood cells and casts can also be increased, and the casts are mainly transparent and granules.

Renal function: Blood urea nitrogen and creatinine are often used to estimate renal function. There was no abnormality in the early patient examination, and the renal parenchyma was damaged to a certain extent and began to rise. Adult creatinine >5mg / dl, the elderly and pregnant >1.2mg / dl suggest kidney damage.

The phenol red excretion test, the urea clearance rate, and the endogenous creatinine clearance rate may be lower than normal.

Diagnosis and diagnosis of malignant small artery and kidney caused by primary malignant hypertension in the elderly

diagnosis

Systemic vasculitis, a group of diseases characterized by inflammation and necrosis of the vessel wall (mainly arteries), including nodular polyarteritis, allergic vasculitis, and granulomatosis (Churg- Strauss disease) Wegner granuloma, giant cell arteritis, Kawasaki disease and Takayasu arteritis, most of which are related to immune mechanisms, such as proteinuria, hematuria, hypertension, renal dysfunction and other kidney damage. Among them, nodular polyarteritis and Wegener's granulomatosis can also be secondary to malignant hypertension, but various systemic vasculitis have their own clinical features (especially extrarenal manifestations), and some difficult cases can be used as kidney The biopsy is clearly diagnosed.

Clinical diagnosis of malignant hypertension and malignant small arteriosclerosis, such as the lack of essential hypertension and chronic glomerulonephritis history, hypertension and urinary abnormalities have been unclear, then judge this malignant hypertension and malignant arterioles Whether kidney cirrhosis is caused by primary hypertension or chronic glomerulonephritis is relatively difficult, younger (under 40 years old), anemia and kidney reduction are beneficial to the diagnosis of the latter, if necessary An open renal biopsy is needed to confirm the diagnosis.

Differential diagnosis

Malignant small arteriosclerosis is mainly identified by the following diseases:

1. Hypertensive crisis patients with high blood pressure, blood pressure rises sharply, headache, dizziness, nausea, vomiting, blurred vision, palpitations, chest tightness, excessive sweating, skin flushing or paleness, etc. . At this time, DBP often exceeds 130 mmHg, the fundus lesions are aggravated, and hypertensive encephalopathy and acute left heart failure can be induced, so it should be differentiated from malignant hypertension. Hypertensive crisis is caused by sympathetic hyperactivity and temporary strong contraction of the small arteries. Therefore, as long as the incentives are removed and the antihypertensive treatment is actively performed, the crisis can be quickly relieved, and the hypertension is obviously easier to control than the malignant hypertension. Blood pressure crisis, if it occurs on the basis of essential hypertension, generally does not cause severe kidney disease. If it occurs on the basis of renal parenchymal hypertension, the renal disease performance may be aggravated (urinary test weight gain, renal function deterioration), However, it is often aggravated, and the crisis can be restored to the original level after the crisis is lifted. These characteristics can be identified with malignant hypertension.

2, rapid glomerulonephritis both hematuria, proteinuria, edema, hypertension and progressive renal dysfunction, can occur oliguric acute renal failure, it is sometimes necessary to identify. However, patients with acute nephritis generally only show moderate hypertension, no hypertensive heart and brain complications, and necroinflammatory changes in the fundus. Pathological examination of more than half of the glomeruli has large crescents (malignant small arteriosclerosis Symptoms often only a small amount of crescents, and no malignant hypertensive small arterial lesions, these characteristics can be identified.

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