Benign arteriosclerosis caused by essential hypertension in the elderly

Introduction to benign small arteriosclerosis caused by essential hypertension in the elderly The disease is common, caused by systemic hypertension, and is the second disease (about 25%) that causes end-stage renal failure in Western countries. The incidence rate in China is also increasing. The disease can be divided into benign small arteriosclerosis (benignarteriolarnephrosclerosis) and malignant arteriolarnephrosclerosis (malignantarteriolarnephrosclerosis). basic knowledge The proportion of sickness: 0.01% Susceptible people: the elderly Mode of infection: non-infectious Complications: arteriosclerosis

The cause of benign small arteriosclerosis caused by essential hypertension in the elderly

Causes:

Benign small arteriosclerosis is caused by long-term uncontrolled high-grade hypertension. The higher the blood pressure and the longer the duration, the heavier the lesion. The arterial lesions are mainly the hyaline wall of the afferent arterioles, and the thickening of the interlobular arteries and the intima of the arcuate artery wall, which cause ischemic renal parenchymal damage.

Pathogenesis:

1. Pathology generally sees bilateral kidney symmetry, normal size or mild to moderate reduction, severely reduced in rare, early surface normal, followed by fine granular irregularities, normal renal pelvis and renal pelvis system, two kinds of mirrors have certain Characteristics of small arterial lesions:

(1) myointimal hypertrophy: often occurs in the arcuate artery and interlobular artery, and the latter is most obvious, the performance of the internal elastic membrane double track sign and the middle layer of hypertrophy.

(2) Glass-like change: the most obvious small artery into the ball, thickened glassy material on the wall, filled with uniform eosinophil-like substance, atrophy of the smooth muscle cells, narrow lumen, glass-like traits A large amount of glycoprotein and collagen traits, so PAS staining positive, using immunofluorescence technology can be found in the glassy area of IgM, C1 and C3 sedimentation, as seen in animal models, glass-like substances are high blood pressure caused by blood vessels After the infiltration of blood components after the wall permeability is enhanced, Kashgarin concludes that the glass-like traits are derived from three pathways:

1 Plasma macromolecular substances invade the blood vessel wall through the inner membrane.

2 The extracellular matrix synthesis of the vessel wall is increased.

3 Impaired endothelial cells, smooth muscle cells and basement membrane fusion, it seems that Kashgarin's point of view seems more comprehensive.

Hypertension-induced small arteriosclerotic lesions can spread throughout the body, but the kidney is most obvious. This may be because the renal artery communicates directly with the abdominal aorta, and the renal blood flow is very large (accounting for 25% of the cardiac output per unit time). The high-pressure blood flow must have a greater impact on the intrarenal arterioles, and the degree of sclerosis of the renal arteries is generally parallel to the hardening of the retina and pancreatic arterioles.

The interlobular artery and the afferent arterioles are often the only findings in the renal pathological section of patients with essential hypertension (glomerulus and tubular normal), so it may represent the earliest manifestation of hypertensive renal vascular damage. This is consistent with what is seen in the animal model.

When small arterial lesions, tube wall thickening, lumen stenosis develops to a certain degree of severity, glomerular blood supply is significantly reduced, sputum causes glomerular and tubular ischemic lesions, the former manifested as glomerular capillaries Wrinkling collapse, capillary wall thickening, mesangial matrix increase, glomerular wall thickening, glomerular atrophy becomes smaller, and even the entire sclerosis, due to the blood supply of the renal tubules The glomerulus is more sensitive to ischemia, so the renal tubular lesion precedes the glomerulus, the early turbid swelling, the tubular atrophy, the basement membrane thickening, and renal interstitial fibrosis.

The glomerular sclerosis and the contraction of interstitial fibrous connective tissue cause depression on the surface of the kidney, compensatory hypertrophy of the normal glomerulus, and compensatory hypertrophy and expansion of the renal tubule, causing the surface of the kidney to bulge. Many fine particles on the surface of the kidney seen by the naked eye are formed.

Mild arteriolar glassy changes can be found in the autopsy of normal elderly without hypertension; diabetic patients can also have renal arterioles, but it involves both the occlusion and the efficacies, which is high. Blood pressure mainly affects the small arteries of the ball; young non-diabetic kidney biopsy found that small arterial glassy changes should consider the disease because of high blood pressure, but can not be used to identify whether this hypertension is primary or secondary, from the light microscope and Electron microscopy showed no difference in renal vascular damage caused by essential hypertension and renal vascular hypertension caused by renal vascular hypertension (due to renal artery stenosis).

Tracy et al. performed a quantitative pathological analysis of the degree of renal arteriosclerosis in hospitalized death cases with at least several years of hypertension records, and then summarized them by multiple regression methods. The results showed that the degree of renal arteriosclerosis (small arteriolar endometrium) Hypertrophy and degree of glassy change as indicators) are significantly different from the degree of hypertension in the weeks to months before death, and have nothing to do with previous blood pressure (low or higher), some patients (especially cancer patients) The blood pressure is normal for a considerable period of time before death, and the degree of renal arteriosclerosis is mild (regardless of the degree of hypertension in the past), which indicates that benign small arterial lesions caused by hypertension are at least partially possible after hypertension is corrected. restore.

Combining the above and animal experiment results, primary hypertension due to:

1. The course of the disease itself is slow.

2. Compensatory middle layer hypertrophy of renal arterioles may inhibit the further development of its glassy changes.

3. Intramuscular hypertrophy and hyalinization may partially recover when blood pressure tends to be stable during the course of the disease. and so:

(1) Its renal arteriolar lesions have not developed enough to cause glomerular and tubular ischemic pathological changes for a long period of time (average of at least 15 years according to Perera's statistics).

(2) Even if ischemic glomerular and tubular lesions occur, and even renal insufficiency occurs, its development is slow (may not progress after the blood pressure is satisfactorily controlled), and end-stage uremia rarely occurs. Or most of the patients who have died of uremia have died of cerebral vascular complications.

2. Pathophysiology

Later, Alba et al. combined clinically to summarize renal function and pathological changes during the course of essential hypertension:

The first stage (early stage): mildly elevated but unstable blood pressure; increased renal blood flow (RBF) and glomerular filtration rate (GFR), sodium diuresis after salt load, and renal artery wall may appear Regular follicular glassy material deposition, glomeruli are generally normal.

The second stage (interim): the blood pressure continues to increase steadily, but the diastolic blood pressure does not exceed 14.7 kPa (110 mmHg); the RBF is reduced to a certain extent, the renal tubule is sensitive to ischemia, and there may be mild damage, which is characterized by N-acetyl in urine. -B-glucosidase (NAG), 2 microglobulin excretion increased; GFR is generally normal, increased filtration fraction, common glassy changes in renal arterioles, intermediate hypertrophy and fibrosis in interlobular arteries, but the inner diameter is not Narrowing, glomerular and tubular can have mild ischemic changes: localized capillary wall thickening and capillary vasoconstriction, focal tubular atrophy, basement membrane thickening, division, and hardening, which is often Part of systemic atherosclerosis, but not necessarily the degree of atherosclerosis in other parts of the body, the majority of patients are elderly, renal vascular stenosis can cause renal vascular hypertension and renal ischemia, the main branch is narrow The renal parenchymal ischemic fibrosis in the blood supply range can cause obvious scarring of the kidney surface; patients may have a small amount of proteinuria, renal insufficiency may also occur, and essential hypertension causes kidney Arteriosclerosis promotes atherosclerosis, Vetrorec provides coronary and abdominal angiography in 200 hypertensive patients (mean age 57 years), and 21 (11%) renal artery stenosis (tube diameter narrowing > 50) %), so it should be noted that the second disease can exist at the same time. Clinically, common elderly people develop mild azotemia under stress and fever. At this time, urine protein is checked, or negative or only a small amount, the patient does not There must be a history of hypertension, which is mostly the coexistence of senile kidney, renal atherosclerosis and renal arteriosclerosis.

Pathological diagnosis: If the clinical diagnosis is difficult, it can be used for renal biopsy. The pathology is consistent with benign small arteriosclerosis caused by essential hypertension. The degree of renal arteriosclerosis and glomeruli, renal tubules and interstitial ischemia and fibrosis The degree of lesions is consistent, but the cause of hypertension and small arteriosclerosis, renal puncture is easy to bleed, need to pay attention (especially elderly patients).

Prevention of benign small arteriosclerosis caused by essential hypertension in the elderly

1. Open mind, optimistic spirit, pay attention to work and rest, actively participate in cultural and sports activities, mental workers insist on doing certain physical activities, etc., which is conducive to maintaining the normal function of the advanced nerve center; no smoking, less salt; avoid getting fat; It has positive significance in preventing this disease.

2. Carry out mass prevention and treatment work, carry out collective regular health checkups, and have a history of hypertension with a family history of hypertension, and regular follow-up observations are conducive to the early detection of this disease and Early treatment.

3. Advocate that each physician will measure blood pressure as a routine examination at the time of diagnosis, which will help to identify asymptomatic early hypertensive patients and provide them with opportunities for early treatment.

In addition, it also attaches importance to factors affecting renal damage in patients with essential hypertension, such as gender, race, diabetes, hyperlipidemia and hyperuricemia, and prevention and treatment of primary hypertension and kidney damage, not only focusing on effectiveness and satisfaction. In order to control high blood pressure, we must consider various other factors that can damage the kidney and treat them accordingly.

(1) Gender: In the same high blood pressure level, the pre-menopausal women have higher heart rate than men, and the peripheral vascular resistance is lower (no difference after menopause). Men are more prone to hypertensive vasculopathy; Tierney et al. Multivariate regression analysis of internal medicine outpatients found that high blood sugar can be controlled, the height of systolic blood pressure and male factors have an impact on renal dysfunction.

(2) Race: The incidence of hypertension in African Americans is twice that of Caucasians; black blood pressure is prone to renal vascular resistance; blacks are a special risk race for end-stage renal disease.

(3) Diabetes: Essential hypertension and diabetes are common diseases of the internal medicine, and the incidence of the disease is 4.67% in the country and 7.73% in the case of critical hypertension. The prevalence of the latter 6.74%), both diseases often involve genetic factors (the former has a family history of 40% to 60%, the latter accounted for 8.7%), generally begin to occur in middle age, the incidence increases with age, so they Often accompanied by clinically, there are high blood pressure first and then diabetes, and of course the opposite.

Essential hypertension is often accompanied by abnormal glucose metabolism, which is expressed as resistance to insulin; Reaven combines hypertension with islet resistance, impaired glucose tolerance, hyperinsulinemia, elevated low-density lipoprotein and triglyceride, and High-density lipoprotein cholesterol levels are reduced by "X syndrome"; Kaplan believes that: obesity, impaired glucose tolerance, hypertriglyceridemia and high blood pressure, the deadly quadruple syndrome has a common pathogenesis, that is, may be associated with insulin Resistance related.

Hyperglycemia caused by impaired glucose tolerance is an important factor causing diabetic kidney damage. It is also suggested that insulin has a direct effect on microvessels; hyperglycemia increases blood volume, increased cardiac output, and hyperinsulinemia promotes renal tubular absorption of sodium. Increased, sodium-rich blood vessels stimulate the sympathetic nerves, which promotes higher blood pressure. If diabetic nephropathy occurs, it will undoubtedly further aggravate kidney damage and high blood pressure.

(4) Hyperlipidemia: Essential hypertension is often accompanied by hyperlipidemia, both of which have an increase in erythrocyte membrane sodium-potassium reverse transfusion, which may be related to genetic factors, while sodium-potassium reversed transfusion Both the increase and the increase in blood lipids can be the result of abnormal intracellular lipid metabolism.

In 1982, Moorrhead et al first proposed the concept of lipid nephrotoxin. In recent years, research on abnormal lipid metabolism to promote the progression of kidney disease has received increasing attention. Many evidences suggest that abnormal lipid metabolism can progress to glomerular sclerosis through mesangial injury, resulting in immunity. And the persistence and progression of non-immune kidney disease, Li Jingzi and other single kidney nephrectomy rats with high cholesterol diet can cause widening of the mesangial area, and found that the excretion of urine protein increases with the increase of mesangial, and Lipid-lowering drugs can significantly reduce mesangial widening and significantly reduce urinary protein excretion; Zhang Jinghong et al found that Chinese medicine rhubarb may improve progressive lipid damage, glomerular sclerosis and functional changes caused by lipid abnormalities by adjusting lipid metabolism. The role of treatment for chronic renal failure.

(5) hyperuricemia: in the first stage of essential hypertension, renal blood flow can be reduced to a certain extent, due to mild damage to the ischemic sputum of the renal tubule, manifested as uric acid secretion disorder and high Uric acidemia, according to statistics, 26% to 33% of untreated patients with mild essential hypertension have hyperuricemia, whereby hyperuricemia can be used as an early renal damage in essential hypertension In 1980, Messerli et al further measured glomerular filtration rate, renal and systemic hemodynamics and blood volume in patients with essential hypertension during critical and stable periods, and found that blood uric acid concentration was negatively correlated with renal blood flow. It is positively correlated with renal and systemic peripheral vascular resistance, but not with cardiac output, heart rate, blood volume and glomerular filtration rate, suggesting that hyperuricemia may further represent its early renal vascular damage.

4. Weight loss: Weight gain is closely related to hypertension. Weight loss in patients with hypertension is beneficial to improve insulin resistance, diabetes, hyperlipidemia and left ventricular hypertrophy. It can strengthen physical activity by reducing daily calorie and salt intake. The method is reached.

5. Exercise: Exercise can not only reduce systolic and diastolic blood pressure (6 ~ 7mmHg), but also help to lose weight, enhance physical strength, and reduce insulin resistance. You can choose jogging, brisk walking, Tai Chi, etc. according to age and physical condition. Mode, the frequency of exercise is generally 3 to 5 times a week, each lasting 20 to 60 minutes.

6. Qigong and other biological behavior methods: Qigong is a traditional Chinese health care method. It plays a self-adjusting role through the induction of mind and the adjustment of breath. Long-term Qigong exercise can control blood pressure better, reduce the amount of antihypertensive drugs, and can make The incidence of stroke is reduced.

Complications of benign small arteriosclerosis caused by essential hypertension in the elderly Complications arteriosclerosis

Common retinal arteriosclerosis and hemorrhage, exudation and hypertensive heart disease, cerebrovascular disease and so on.

Symptoms of benign small arteriosclerosis caused by essential hypertension in the elderly Common symptoms Hyperuricemia Heart failure Proteinuria into the aorta Glassy hypertensive Renal damage Left ventricular hypertrophy Chronic renal failure Renal ischemic sclerosis

Whether benign hypertension causes renal arteriosclerosis is first related to the degree and duration of hypertension (especially systolic blood pressure). In general, hypertension must last 10 to 15 years before clinical manifestations of renal damage occur. The following factors can also affect the occurrence of benign small arteriosclerosis: gender (men are more susceptible to morbidity); age (elderly susceptible to morbidity); race (black people are more susceptible); hypertension complications (concurrent diabetes) Hyperlipidemia or hyperuricemia is more likely to occur).

The renal tubule is more sensitive to ischemia, so the earliest clinical symptoms are often nocturia (nocturnal urine volume more than 1/2 of the whole day urine volume is nocturia, is a manifestation of renal tubular dysfunction), at this time, determination of renal blood Flow and urine osmotic pressure (reflecting renal tubular concentrating function) have been reduced to varying degrees, but creatinine clearance (the most sensitive glomerular function test) is still normal, urine routine test protein and microscopic examination are negative, some scholars have found that At this time, if the urinary albumin is detected by sensitive immunological methods, the urinary albumin excretion rate is often increased, but its clinical significance is still unclear. Because of some patients with low medical history, blood pressure is significantly increased when urinary albumin Excretion also increased, and blood pressure control returned to normal, so many scholars believe that this urinary albumin excretion rate is increased, does not reflect glomerular ischemic lesions, but is a change in hemodynamics in the glomerulus (hypertension) Caused by increased glomerular internal pressure).

When glomerular ischemic lesions occur, the protein begins to appear in routine urine tests, and mild microscopic abnormalities (small amount of red blood cells and granular casts) appear in the sediment microscopy. Urinary proteins caused by ischemic glomerular lesions are generally not More often than 1g/d, but when the high blood pressure is high, the glomerular internal pressure is also increased, and the urinary protein excretion can significantly exceed this amount. However, it still does not reach a large amount of proteinuria (3.5g). /d) Category.

As the disease progresses further, creatinine clearance (Ccr) will decrease, renal insufficiency will occur, and when Ccr falls by more than half, renal insufficiency decompensation, serum creatinine (Scr) and urea nitrogen (BUN) increase, after which The disease progresses faster until it finally enters uremia with chronic renal failure. Like other kidney diseases, renal anemia will occur in patients with renal insufficiency, but the anemia of this disease seems relatively light.

At the same time as renal damage, benign hypertension often causes damage to other target organs. Patients often have hypertensive retinopathy (retinal arteriosclerosis, bleeding, exudation, etc.), hypertension, and brain complications.

In addition, renal damage caused by hypertension can in turn act on systemic hypertension. After the occurrence of benign small arteriosclerosis, renal ischemia is aggravated, which will further activate the renin-angiotensin-aldosterone system, which will increase systemicity. High blood pressure, forming a vicious circle.

Examination of benign small arteriosclerosis caused by essential hypertension in the elderly

Serum creatinine, increased urea nitrogen, abnormal urine proteinuria, a small amount of red blood cells and granular casts.

B-mode ultrasonography showed a reduction in the size of the kidneys, which is helpful for diagnosis.

Diagnosis and diagnosis of benign small arteriosclerosis caused by essential hypertension in the elderly

Diagnostic criteria

In summary, the necessary conditions for diagnosis:

1 is essential hypertension.

2 There is generally more than 5 years of persistent hypertension before proteinuria occurs (the degree is generally >20.0/13.3 kPa (150/100 mmHg).

3 There is persistent proteinuria (generally mild to moderate), and there are few forms in the microscopic examination.

4 have retinal arteriosclerosis or arteriosclerotic retinal changes.

5 Excluding various primary kidney diseases.

6 Except for other secondary kidney diseases.

Auxiliary or reference conditions:

1 age is over 60 years old.

2 have hypertensive left ventricular hypertrophy, coronary heart disease, heart failure.

3 have a history of cerebral arteriosclerosis and/or cerebrovascular accident.

4 blood uric acid increased.

5 renal tubular dysfunction precedes glomerular dysfunction.

6 The course of disease progressed slowly.

Differential diagnosis

Benign small arteriosclerosis should be differentiated from the following diseases:

1. Chronic glomerulonephritis secondary hypertension: if the medical history is very clear, there is no difficulty in identification, patients with chronic glomerulonephritis have abnormal urine, hypertension is later; and patients with benign small arteriosclerosis have hypertension. Before the kidney damage for more than 10 years, for cases with unclear medical history, especially in patients with renal insufficiency, identification is often very difficult. At this time, the data in Table 1 can be used as a reference for identification.

2. Chronic pyelonephritis secondary to hypertension: most of the patients are women, often with intermittent urinary tract irritation, urinary leukocytosis, positive bacterial culture, and then renal damage (tubular damage often compared with glomerular function) Significant damage) and hypertension, pyelography showed abnormal kidney morphology, renal cortical scar and/or pyelectasis, deformation, because chronic pyelonephritis is mostly unilateral kidney disease, so B-ultrasound is often not the size of the two kidneys Equal, the affected side of the kidney becomes smaller; radionuclide renal dynamic imaging examination of the two kidney glomerular filtration rate and kidney map are also often inconsistent, the affected side of renal function, urinary tract infection history, hypertension occurs after urinary abnormalities and two Renal imaging and functional inconsistency can be distinguished from benign small arteriosclerosis.

3. Renal artery stenosis secondary to hypertension; renal artery stenosis is caused by arteritis, fibromuscular dysplasia or atherosclerosis, the former two occur in young people, the latter is more common in the elderly, patients often appear severely high Blood pressure, up to 200/120mmHg, diastolic blood pressure increased significantly, and then mild urine abnormalities (mild urine protein and formed points), and finally the renal function gradually declines, the patient's abdomen can sometimes smell systolic or double-phase murmur, B-ultrasound examination of the affected side of the kidney shrinkage, renal venous blood test side of the affected side of renin activity increased, captopril radionuclide kidney chart test, renal angiography found that the trunk or branch stenosis can confirm the disease, the degree of hypertension is serious, Kidney damage appeared earlier, the two kidneys showed inconsistent imaging and function, and were different from benign small arteriosclerosis, and renal angiography could identify the two diseases.

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