Renal parenchymal hypertension

　　First, Causes of Disease

　　Many renal parenchymal diseases can cause hypertension, and the incidence of hypertension varies among different renal parenchymal diseases.

　　1. Unilateral renal parenchymal diseases that can cause hypertension:Including reflux nephropathy, chronic pyelonephritis, hydronephrosis, and renal adenocarcinoma, etc. If the detection finds that the venous blood renin level on the affected side of the kidney is high, early resection of the affected kidney may cure or significantly improve hypertension. Hypertension is common in patients with congenital unilateral renal agenesis (kidney not developed), while hypertension does not increase in patients with acquired unilateral nephrectomy (resection of the diseased kidney or as a donor for renal transplantation), and the mechanism is unclear.

　　2. Bilateral renal parenchymal diseases that can cause hypertension:Including primary and secondary glomerular diseases, chronic interstitial nephritis, adult polycystic kidney disease, etc. Generally speaking, the incidence of hypertension in primary and secondary glomerular diseases is higher than that in chronic interstitial nephritis and adult polycystic kidney disease, and the incidence of hypertension is highest in those with proliferative and/or fibrotic pathological changes in primary and secondary glomerular diseases. In addition, regardless of which kidney disease, the incidence of hypertension increases with the appearance of renal function damage. According to literature statistics, more than 90% of patients with end-stage renal disease have hypertension.

　　Second, Pathogenesis

　　The main mechanism of hypertension caused by acute renal parenchymal disease is water and sodium retention, increased blood volume, and diuresis can often lower blood pressure, even to normal levels. However, the pathogenesis of hypertension in chronic renal parenchymal disease is more complex and can be caused by various factors.

　　1, Factors Leading to Sodium Retention and Increased Blood Volume

　　(1) Factors Leading to Increased Blood Volume: The following factors can lead to water and sodium retention: ① Decreased glomerular filtration rate, reduced excretion of water and sodium; ② Activation of the RAAS, aldosterone promotes the reabsorption of sodium by the distal renal tubules and collecting ducts; ③ Activation of the sympathetic nervous system, promotes the reabsorption of sodium by the proximal renal tubules; ④ Decreased production of nitric oxide, reduced excretion of sodium by the renal tubules; ⑤ Impaired renal function leads to insulin resistance, increased insulin levels in the body stimulate the sodium pump (Na-K-ATPase) to increase the reabsorption of sodium by the proximal renal tubules. Obvious water and sodium retention can lead to the occurrence of volumetric hypertension.

　　(2) Mechanisms Leading to Increased Vascular Resistance: The following mechanisms can lead to vasoconstriction of peripheral and renal arteries, increasing vascular resistance: ① Activation of the RAAS, activation of the sympathetic nervous system, and increased synthesis of endothelin stimulate vasoconstriction; ② Decreased NO production, weakened antagonism of vasoconstrictive factors; ③ Decreased GFR leads to increased secretion of parathyroid hormone, extracellular volume expansion stimulates the release of endogenous quinagolide, and both parathyroid hormone and quinagolide can increase intracellular Ca2+ concentration, promote vasoconstriction, and increase the sensitivity of vascular smooth muscle to vasoconstrictive factors; ④ Insulin resistance, high insulin levels stimulate vascular smooth muscle hypertrophy, enhance vascular responsiveness, thicken the vessel wall, narrow the lumen, and increase vascular resistance. These factors can all lead to resistive hypertension.

　　In renal实质性 hypertension, both pure volumetric hypertension and pure resistive hypertension are rare, and the vast majority of patients have both pathogenic factors. Compared with essential hypertension, the volume factors in renal实质性 hypertension are often more prominent.

　　From the above description, it can be seen that the occurrence of both volumetric and resistive hypertension is related to the participation of many neurohumoral factors, as summarized briefly in Table 2.

　　2, Factors Leading to Hypertension

　　(1) Activation of the Renin-Angiotensin-Aldosterone System (RAAS): A large amount of evidence has confirmed that RAAS plays an important role in the occurrence and development of renal实质性 hypertension. Ischemia during renal parenchymal disease can lead to the activation of RAAS. Angiotensin II can directly stimulate vasoconstriction and also increase sympathetic nervous system activity centrally and at the endings of sympathetic nerves, promoting the release of catecholamines, further causing vasoconstriction; aldosterone can increase the reabsorption of sodium by the distal renal tubules and collecting ducts, exacerbating water and sodium retention. Therefore, the activation of RAAS can participate in both resistive and volumetric hypertension.

　　(2) Enhanced Sympathetic Nervous System Excitability: The sympathetic nervous system also plays an important role in the pathogenesis of renal实质性 hypertension. During renal parenchymal disease, the sympathetic nervous system can be activated through renal reflexes, and the increase in AⅡ will also increase its activity centrally and peripherally. The activation of the sympathetic nervous system can stimulate vasoconstriction, increase vascular resistance; it can promote the reabsorption of sodium by the proximal renal tubules, increase blood volume, and thus participate in the occurrence of hypertension from both resistance and volume aspects. The activation of the sympathetic nervous system can also cause vasoconstriction of renal vessels, reduce renal blood flow, and stimulate the secretion of renin, further activating RAAS and aggravating hypertension.

　　(3) Release of endogenous digitalis-like substances: Endogenous digitalis-like substances that can react with digitalis antibodies have the following characteristics: inhibit Na-K-ATPase, promote sodium excretion. When renal parenchymal disease causes extracellular volume expansion, it can reflexively stimulate the hypothalamic brain tissue to release EDIS, inhibit the Na-K-ATPase in the proximal renal tubular epithelial cells, reduce sodium reabsorption, and produce diuresis. However, on the other hand, EDIS will inhibit the Na-K-ATPase in the vascular smooth muscle, increase intracellular sodium concentration, reduce the transmembrane sodium gradient, reduce the exchange of Na/Ca2, and depolarize voltage-dependent Ca2 channels, so that intracellular Ca2 increases, which promotes the occurrence of resistance hypertension.

　　(4) Endothelin: Endothelin is the strongest vasoconstrictor peptide found in the body so far, which may act through endocrine pathways, as well as autocrine and paracrine pathways. Endothelin can stimulate vasoconstriction; promote the activation of RAAS; reduce renal blood flow and GFR, and reduce urinary sodium excretion. Therefore, it may also participate in the onset of renal实质性 hypertension from both resistance and volume aspects.

　　(5) Arginine vasopressin: Arginine vasopressin has little effect on blood pressure in normal organisms and patients with primary hypertension, but clinical trials have shown that the application of arginine vasopressin antagonists to patients with chronic renal failure can effectively lower hypertension, suggesting that arginine vasopressin can participate in the occurrence of hypertension in renal failure patients through vasoconstrictive effects. However, more research is needed to confirm this observation and clarify the mechanism of action.

　　(6) Decrease in antihypertensive factors: The kidneys can produce various antihypertensive factors, such as prostaglandin E2 and I2, kinins (the distal renal tubular epithelial cells produce kinin-releasing enzyme, which then converts kininogen in plasma into kinins), atrial natriuretic peptide, brain natriuretic peptide, NO, and medullary antihypertensive lipids, etc. As mentioned before, when there is renal parenchymal disease, the production of NO decreases, the antagonistic effect on vasoconstriction is weakened, and the reduction of NO can also reduce the excretion of sodium in the renal tubules, exacerbate water and sodium retention, so it can participate in the onset of hypertension from both resistance and volume aspects. However, to date, there is still no conclusive evidence of the participation of other antihypertensive factors in the onset of renal实质性 hypertension.

　　It can be complicated with renal failure, hypertensive encephalopathy and other complications. A pathological condition in which the kidney function is partially or completely lost. It is divided into acute and chronic types according to the severity of the onset. Acute renal failure is a condition in which the excretory function of both kidneys is lost in a short period of time due to various diseases, abbreviated as acute renal failure. Hypertensive encephalopathy is a special clinical phenomenon that occurs in the course of primary hypertension or some secondary hypertension. The treatment principle of hypertensive encephalopathy is to lower the blood pressure as quickly as possible, stop convulsions, reduce brain edema, correct intracranial hypertension, and prevent serious complications.

　　The various symptoms of hypertension are also present in essential hypertension, and will not be elaborated further. Below, only a brief introduction will be given to some special aspects of essential hypertension.

　　Compared with primary hypertension at the same level, essential hypertension is more likely to progress to malignant hypertension, with an incidence about twice that of the latter. Among them, IgA nephropathy, especially proliferative sclerotic or sclerotic IgA nephropathy complicated by malignant hypertension is particularly common, and compared with primary malignant hypertension, renal essential malignant hypertension has a poorer prognosis. Some authors have reported that the 5-year renal survival rate of the former is 60%, while the 1.5-year renal survival rate of the latter is only 4%.

　　The fundus lesions of essential hypertension are often severe, and cardiovascular and cerebrovascular complications are more likely to occur. This is because, in addition to hypertension, there are often other complex cardiovascular risk factors present during renal parenchymal disease, such as lipid metabolism disorders in nephrotic syndrome, glucose metabolism disorders in diabetic nephropathy, anemia in renal insufficiency, hyperuricemia, hyperhomocysteinemia, uremic toxins, metabolic acidosis, and a microinflammatory state, etc. These complex factors will significantly increase the incidence of cardiovascular complications.

　　Here, it is also necessary to emphasize the impact of essential hypertension on the progression of primary kidney diseases, especially chronic glomerulonephritis. During chronic glomerulonephritis, the pre-glomerular arteries are in a dilated state, and systemic hypertension is easily transmitted to the glomeruli, causing high pressure, high perfusion, and high filtration within the glomeruli. These 'three highs' can accelerate the sclerosis of the remaining glomeruli. At the same time, long-term hypertension can lead to arteriosclerosis of the renal small arteries, including hyaline change of the afferent arterioles, thickening of the intima of interlobular arteries and arcuate arteries, which makes the arterial wall thick and the lumen narrow, leading to secondary renal parenchymal ischemia.

　　Damage (glomeruli showing ischemic contraction to ischemic sclerosis, atrophy of renal tubules, and fibrosis of the renal interstitium), so poorly controlled essential hypertension will significantly accelerate the progression of renal parenchymal disease, forming a vicious cycle.

　　In glomerulonephritis with high proteinuria, the renal damage caused by hypertension is more obvious because of the additive effect of the two. It is known that proteinuria, especially large amounts of proteinuria, can cause high pressure within the glomeruli, high perfusion, and high filtration, which promote glomerulosclerosis. Moreover, the filtered proteins (including complement and growth factors, etc.) and certain substances bound to proteins (including lipids and iron, etc.) are reabsorbed by the renal tubules, which can activate renal tubular cells and release pathogenic factors (such as transforming growth factor β, etc.) to promote interstitial fibrosis. Therefore, for patients with essential hypertension complicated by proteinuria, it is even more necessary to strictly control hypertension.

　　Preventing and actively treating primary kidney diseases is the key to preventing and treating essential hypertension. It is advocated to adopt a vegetarian diet as the main dietary approach, as a vegetarian diet can help lower blood pressure in patients with hypertension. Therefore, patients with hypertension should have a light diet, high in vitamins, dietary fiber, calcium, low in fat, and low in cholesterol. The total fat should be less than 30% of the total calories, and protein should account for about 15% of the total calories. It is advocated to eat more coarse grains, mixed grains, fresh vegetables, fruits, soy products, lean meat, fish, and chicken, and to use vegetable oils, while eating less lard, greasy foods, and sugar, spices, strong tea, and coffee.

　　According to the specific renal parenchymal lesions, the laboratory tests have their own characteristics, such as acute glomerulonephritis: hematuria, proteinuria with transient azotemia as the main symptom, chronic glomerulonephritis: a large amount of protein in the urine, often with red blood cells and casts, anemia and renal function damage, chronic pyelonephritis: with a history of urinary tract infection,微量or a small amount of protein, a small amount of red blood cells and white blood cells, urine bacterial culture positive.

　　1. Kidney ultrasound:The kidneys show diffuse lesions, with the renal cortex becoming thin, etc.; there are corresponding imaging characteristics of primary diseases.

　　2. Fundus examination:There may be changes such as retinal hemorrhage, exudation, and papilledema.

　　Dietary adjustment principles for hypertension and kidney disease

　　1. Control the supply of the three major nutrients

　　The intake of carbohydrates and other calories should not cause overweight; fat intake should consume vegetable oils and control the intake of animal fats; the protein intake should be adjusted according to the condition. For patients with normal renal function and large protein loss in urine, it is necessary to provide foods rich in nutrition and high-quality protein, such as milk, eggs, lean meat, fish, etc. For patients with renal insufficiency, protein intake should be limited, and 0.5-0.8 grams per kilogram of body weight can be supplied daily.

　　2. Control the intake of salt

　　The daily intake of sodium salt, including the sodium content in food, should be controlled within 3-5 grams.

　　3. Eat more hypotensive, diuretic, and fat-reducing foods

　　Foods with good diuretic effects, such as loofah, luffa, Job's tears, red bean, corn silk, etc. Foods with good hypotensive effects are mostly foods rich in potassium and calcium, such as mushrooms, mushrooms, lotus seeds,玉兰片, kelp, seaweed, spinach, etc., which have a high potassium content; such as celery, shepherd's purse, sesame, tofu, shrimp paste, shrimp, etc., which have a high calcium content. Foods with lipid-lowering effects include milk, soybeans, mung beans, corn, bran, oatmeal, sunflower seeds, peanuts, black fungus, mushrooms, shiitake mushrooms, celery, garlic, onions, ginger, kelp, tea, etc.

　　4. Quit smoking and avoid excessive alcohol consumption

　　Patients with hypertension and kidney disease must quit smoking and avoid excessive alcohol consumption. The appropriate calorie intake should be determined according to the condition, generally with maintaining an ideal body weight as the standard. Since these patients often have lipid metabolism disorders, reducing fat intake not only helps control calorie intake but also improves metabolic disorders. Under the guidance of a doctor, analyze your diet, change bad eating habits, limit certain foods, and only in this way can you meet the nutritional requirements and improve the quality of life.

　　I. Treatment

　　The treatment principles for hypertension caused by various nephropathies are basically consistent.

　　1. Control of water and salt intake:To reduce blood volume, but attention should be paid to excessive reduction of blood volume, which can worsen renal function.

　　2. Diuretics:Thiazides are commonly used drugs, but when the creatinine clearance rate is below 30ml/min, the diuretic effect is significantly reduced, and furosemide (Lasix) and ethacrynic acid (Edecrin) should be used instead, and potassium-sparing diuretics should be contraindicated in azotemia.

　　3. Antihypertensive treatment:The application of angiotensin-converting enzyme inhibitors (ACEI) and calcium antagonists in renal实质性 hypertension has received widespread attention. ACEI not only inhibits the degradation of angiotensin II and kinins but also dilates the efferent arterioles, relieves the increased pressure within the glomeruli, and reduces the damage to the glomeruli. Captopril is particularly beneficial for rapidly progressive hypertension. Other drugs such as hydralazine (hydralazine), minoxidil (Minoxidil) are also effective in controlling hypertension in renal insufficiency.

　　4. Hemodialysis:For patients with renal failure who are ineffective to drug treatment, hemodialysis is often required, and antihypertensive drugs do not need to be discontinued during dialysis, and the effect of minoxidil is relatively satisfactory.

　　II. Prognosis

　　Chronic glomerulonephritis azotemia and renal实质性 hypertension often suggest poor prognosis. Although general antihypertensive drugs can reduce peripheral vascular resistance, they may not necessarily reduce glomerular vascular resistance. Long-term effective antihypertensive treatment can repair small artery lesions and has a certain effect on preventing cardiovascular and cerebrovascular complications, but the effect of antihypertensive treatment is poor. Calcium antagonists such as nifedipine can lower blood pressure, but they increase the resistance of the efferent arterioles, thereby increasing the pressure within the glomeruli, which is unfavorable for renal function protection. It is now recognized that angiotensin-converting enzyme inhibitors not only reduce peripheral vascular resistance but also inhibit the renin-angiotensin system in the tissues, reducing the degradation of bradykinin in the tissues, preventing vascular wall thickening and smooth muscle hyperplasia. Angiotensin II receptor antagonists used in recent years, either alone or in combination with ACE inhibitors, have also achieved good results. The following indications are suitable for nephrectomy surgery: ① Unilateral renal lesion; ② Renal function less than 20% of total function; ③ Difficult to control hypertension; ④ Recurrent urinary tract infection.