The Harm of Drinking in Nephrotic Syndrome Patients

The Harm of Drinking in Nephrotic Syndrome Patients

Nephrotic syndrome should limit drinking. Drinking can lead to increased obesity, decreased glycogen synthesis. Particularly in obese, hypertensive, nephrotic syndrome and hyperlipidemic patients. Excessive alcohol consumption can decrease appetite, food intake decreased, resulting in a variety of nutrient deficiencies, severe alcoholic cirrhosis can occur. Nephrotic syndrome patients should avoid alcohol, because alcohol can reduce renal blood flow, deterioration of renal function, and increase the burden on the heart.

Prevention of nephrotic syndrome should pay attention to infection. Nephrotic syndrome patients with low resistance, prone to infection. Patients with nephrotic syndrome should be noted that ventilation ventilation, often take a bath, keep the skin clean, to prevent urinary tract infections, pay attention to rest, cold seasonal precautions to prevent a cold, infection occurs in time for the treatment of nephrotic syndrome.

Patients with nephrotic syndrome, a small amount of alcohol is good for the body, can enhance the protection of the body against UV damage, etc., but here is a small amount of very few, about a day into a few grams of alcohol, the general amount of alcohol can not be so Less, the amount is difficult to control, so for their own health. Patients with nephrotic syndrome is best not to drink, wine can not drink, life will not cause a big impact, there is no healthy body, you can not better enjoy the beauty of life.

what can cause nephrotic syndrome

Is nephrotic syndrome harmful?

Kidney disease experts pointed out that the severity of nephrotic syndrome manifested as renal failure, uremia. In the early stages of nephrotic syndrome, if there is no effective measures to treat it, nephrotic syndrome will cause serious harm to the human body, to people's normal life and work caused a lot of inconvenience. Timely and correct treatment of the disease, so that patients get rid of nephrotic syndrome as soon as possible, with a healthy body.

When the nephrotic syndrome occurs, accompanied by nephrotic patients will occur a series of concurrent symptoms, edema, hyperlipidemia, anemia and so on. These symptoms indicate that the body resistance of patients decreased, while the body's immune regulation system has undergone tremendous changes, which will lead to abnormal expression of the body's protein, resulting in the emergence of hypoproteinemia. Nephrotic syndrome Hypoproteinemia is not only a direct impact on the body's protein needs, but also on the body there are other aspects. The human body is a complex body, its various symptoms are interrelated, mutual influence.

Due to the excretion of large amounts of proteinuria, inadequate supply of synthetic protein in the liver, leading to hypoproteinemia. The emergence of this phenomenon is a very serious nephrotic syndrome hazards. Reduce the blood protein, it will lead to decreased plasma colloid osmotic pressure, colloid osmotic pressure drop imbalance, the water will overflow within the plasma, and accumulation to the organization and body cavity, resulting in a high degree of human edema. At the same time, when the plasma water spills out, the water content in the blood decreases, and the blood volume in the active circulation is insufficient. Therefore, when the blood is reduced in water, it causes a high blood viscosity, easily forms a blood clot, Ischemia and hypoxia. The emergence of these symptoms will aggravate the process of kidney disease.

Nephrotic syndrome This disease is very high in the incidence of children in the group will have a very negative impact on the growth of children. The incidence of nephrotic syndrome is getting higher and higher, which has aroused widespread concern. Whether it can cure this disease has become one of the concerns of many patients.

What are the complications of nephrotic syndrome in children

What are the complications of nephrotic syndrome in children

Symptoms of nephrotic syndrome in children is mainly a large number of proteinuria, and then hypoproteinemia, hyperlipidemia and varying degrees of edema, edema of children with nephrotic syndrome can be both lower limb edema, nephrotic syndrome in children with common complications Disease specific description is as follows:

(1) infection: due to a large number of immunoglobulin from the urine loss, plasma protein decreased, affecting antibody formation. Adrenal cortex hormones and cytotoxic substances used, so that the patient's body resistance decreased, prone to infection, such as skin infections, primary peritonitis, respiratory infections, urinary tract infection, and even induced sepsis.

(2) coronary heart disease: pediatric nephrotic syndrome patients often hyperlipidemia and hypercoagulable state of the blood, so prone to coronary heart disease. It was reported nephrotic syndrome in patients with myocardial infarction incidence of 8 times higher than normal. Coronary heart disease has become the third cause of nephrotic syndrome death (second only to infection and renal failure).

(3) thrombosis: pediatric nephrotic syndrome in patients prone to thrombosis, in particular, the incidence of membranous nephropathy up to 25% to 40%. The formation of thrombosis due to edema, less patient activity, venous stasis, hyperlipidemia, blood viscosity increased viscosity, high levels of fibrinogen and v, Ⅶ, Ⅷ, x factor increased and the use of adrenal cortex hormones and blood-prone Hypercoagulable state.

(4) acute renal failure: children with nephrotic syndrome due to a large number of proteinuria, hypoproteinemia, hyperlipidemia, the body often in low blood volume and hypercoagulable state, vomiting, diarrhea, the use of anti-hypertensive and Diuresis diuresis, a large number of diuretic, renal blood perfusion can make a sudden decrease, thereby reducing the glomerular filtration rate, leading to acute renal failure. In addition, nephrotic syndrome, renal interstitial edema, protein concentration of tubulointerstitial tubular obstruction and other factors, can also induce acute renal failure.

(5) electrolyte and metabolic disorders: repeated use of diuretics or long-term unreasonable ban salt, can cause children with nephrotic syndrome secondary to hyponatremia; the use of adrenal cortex hormones and a large number of diuretics lead to a large number of urination, Potassium, prone to hypokalemia.

These are Xiaobian to introduce the complications of nephrotic syndrome in children, through the above complications, I hope parents and friends must learn more about nephrotic syndrome, so that early detection and early treatment, try to avoid the occurrence of these complications The harm to the child.

Hypertension Treatment

Hypertension Treatment

Approach Considerations

The 2016 American Diabetes Association's (ADA's) standards of medical care in diabetes also indicate that a majority of patients with diabetes mellitus have hypertension. In patients with type 1 diabetes, nephropathy is often the cause of hypertension, whereas in type 2 diabetes, hypertension is one of a group of related cardiometabolic factors.   Hypertension remains one of the most common causes of congestive heart failure (CHF). Antihypertensive therapy has been demonstrated to significantly reduce the risk of death from stroke and coronary artery disease.

Other studies have demonstrated that a reduction in BP may result in improved renal function. Therefore, earlier detection of hypertensive nephrosclerosis (using means to detect microalbuminuria) and aggressive therapeutic interventions (particularly with ACE inhibitor drugs) may prevent progression to end-stage renal disease.

Lifestyle modifications

Lifestyle modifications are essential for the prevention of high BP, and these are generally the initial steps in managing hypertension. As the cardiovascular disease risk factors are assessed in individuals with hypertension, pay attention to the lifestyles that favorably affect BP level and reduce overall cardiovascular disease risk. A relatively small reduction in BP may affect the incidence of cardiovascular disease on a population basis. A decrease in BP of 2 mm Hg reduces the risk of stroke by 15% and the risk of coronary artery disease by 6% in a given population. In addition, a prospective study showed a reduction of 5 mm Hg in the nocturnal mean BP and a possibly significant (17%) reduction in future adverse cardiovascular events if at least one antihypertensive medication is taken at bedtime.

In a study that attempted to formulate a predictive model for the risk of prehypertension and hypertension, as well as an estimate of expected benefits from population-based lifestyle modification, investigators reported that the majority of risk factors have a larger role in prehypertension and stage 1 hypertension than in stage 2 hypertension. The investigators derived multistep composite risk scores by assessing significant risk factors in the progression from prehypertension to hypertension, as well as the regression of prehypertension to normal; they indicated that as the number of risk factors included in intervention programs increases, the size of the expected mean risk score decreases. In men, the 5-year predicted cumulative risk for stage 2 hypertension decreased from 23.6% (in the absence of an intervention program) to 14% (with 6-component intervention); the results were similar in women.

Treatments and drugs

Medications to treat high blood pressure

Thiazide diuretics. Diuretics, sometimes called water pills, are medications that act on your kidneys to help your body eliminate sodium and water, reducing blood volume.

Thiazide diuretics are often the first, but not the only, choice in high blood pressure medications. Thiazide diuretics include hydrochlorothiazide (Microzide), chlorthalidone and others.

If you're not taking a diuretic and your blood pressure remains high, talk to your doctor about adding one or replacing a drug you currently take with a diuretic. Diuretics or calcium channel blockers may work better for black and older people than do angiotensin-converting enzyme (ACE) inhibitors alone. A common side effect of diuretics is increased urination.

Beta blockers. These medications reduce the workload on your heart and open your blood vessels, causing your heart to beat slower and with less force. Beta blockers include acebutolol (Sectral), atenolol (Tenormin) and others.

When prescribed alone, beta blockers don't work as well, especially in black and older people, but may be effective when combined with other blood pressure medications.

Angiotensin-converting enzyme (ACE) inhibitors. These medications — such as lisinopril (Zestril), benazepril (Lotensin), captopril (Capoten) and others — help relax blood vessels by blocking the formation of a natural chemical that narrows blood vessels. People with chronic kidney disease may benefit from having an ACE inhibitor as one of their medications.

Angiotensin II receptor blockers (ARBs). These medications help relax blood vessels by blocking the action, not the formation, of a natural chemical that narrows blood vessels. ARBs include candesartan (Atacand), losartan (Cozaar) and others. People with chronic kidney disease may benefit from having an ARB as one of their medications.

Calcium channel blockers. These medications — including amlodipine (Norvasc), diltiazem (Cardizem, Tiazac, others) and others — help relax the muscles of your blood vessels. Some slow your heart rate. Calcium channel blockers may work better for black and older people than do ACE inhibitors alone.

Grapefruit juice interacts with some calcium channel blockers, increasing blood levels of the medication and putting you at higher risk of side effects. Talk to your doctor or pharmacist if you're concerned about interactions.

Renin inhibitors. Aliskiren (Tekturna) slows down the production of renin, an enzyme produced by your kidneys that starts a chain of chemical steps that increases blood pressure.

Tekturna works by reducing the ability of renin to begin this process. Due to a risk of serious complications, including stroke, you shouldn't take aliskiren with ACE inhibitors or ARBs.

Additional medications sometimes used to treat high blood pressure

If you're having trouble reaching your blood pressure goal with combinations of the above medications, your doctor may prescribe:

Alpha blockers. These medications reduce nerve impulses to blood vessels, reducing the effects of natural chemicals that narrow blood vessels. Alpha blockers include doxazosin (Cardura), prazosin (Minipress) and others.

Alpha-beta blockers. In addition to reducing nerve impulses to blood vessels, alpha-beta blockers slow the heartbeat to reduce the amount of blood that must be pumped through the vessels. Alpha-beta blockers include carvedilol (Coreg) and labetalol (Trandate).

Central-acting agents. These medications prevent your brain from signaling your nervous system to increase your heart rate and narrow your blood vessels. Examples include clonidine (Catapres, Kapvay), guanfacine (Intuniv, Tenex) and methyldopa.

Vasodilators. These medications, including hydralazine and minoxidil, work directly on the muscles in the walls of your arteries, preventing the muscles from tightening and your arteries from narrowing.

Aldosterone antagonists. Examples are spironolactone (Aldactone) and eplerenone (Inspra). These drugs block the effect of a natural chemical that can lead to salt and fluid retention, which can contribute to high blood pressure.

To reduce the number of daily medication doses you need, your doctor may prescribe a combination of low-dose medications rather than larger doses of one single drug. In fact, two or more blood pressure drugs often are more effective than one. Sometimes finding the most effective medication or combination of drugs is a matter of trial and error.

What are the main hazards of nephrotic syndrome?

What are the main hazards of nephrotic syndrome?

Kidney is one of the body's five internal organs, its health or not completely affect the health of the human body. Nephrotic syndrome is a more serious form of kidney disease. We do not know much about this disease in our lives, and its severity is manifested in the fact that it causes many other diseases and can lead to other diseases in the human body. The normal operation of the system.

What are the main hazards of nephrotic syndrome?

1, nephrotic syndrome in the course of the disease a large number of immunoglobulin from the urine will be lost, plasma protein decreased, affecting antibody formation. Adrenal cortical hormones and cytotoxic drug applications, the patient's body resistance decreased, prone to infection, such as skin infections, primary peritonitis, respiratory infections, urinary tract infection, and even induce sepsis.

2, nephrotic syndrome will induce cardiovascular and cerebrovascular diseases, nephrotic syndrome patients usually have symptoms of hypertension, hypertension is also one of the symptoms of nephrotic syndrome, or cause a lot of important factors of disease, we must not overlook the , Nephrotic syndrome in patients with severe hypertension, easily lead to cardiovascular and cerebrovascular diseases and so on. Therefore, the harm caused by high blood pressure can not be overlooked.

3, the incidence of nephrotic syndrome often have hyperlipidemia or hypercoagulable state of the blood, which easily lead to patients with coronary heart disease. According to some reports, the incidence of myocardial infarction in patients with nephrotic syndrome is higher than the normal people more than 8 times. This is a major risk of nephrotic syndrome.

4, nephrotic syndrome will cause serious damage to the regulatory mechanism, according to the survey of experts, patients with nephrotic syndrome are generally a large number of proteinuria and severe edema symptoms, to the patient's physical and mental health are caused great harm . As the onset of nephrotic syndrome hidden, if symptoms can not be timely treatment, leading to disease spread. As patients with nephrotic syndrome, there will be proteinuria, hypoproteinemia, hyperlipidemia, edema, renal regulation of the mechanism of serious damage.

5, nephrotic syndrome, what is the main hazards, nephrotic syndrome patients due to a large number of hyperlipidemia, proteinuria, hypoalbuminemia, resulting in the body is often in the low blood volume and hypercoagulable state. Vomiting, diarrhea, the use of antihypertensive drugs and a large number of diuretic diuretics, can cause a sudden decrease in renal blood perfusion, thereby reducing the glomerular filtration rate, leading to acute renal failure.

6, nephrotic syndrome is generally can lead to the emergence of acute renal failure. This is due to nephrotic syndrome, renal interstitial edema, protein concentration of the formation of the tubular plug the renal tubular and other factors, can induce acute renal failure. This is a common nephrotic syndrome, the main hazards.

Nephrotic syndrome in the pathogenesis often accompanied by symptoms of other diseases, resulting in nephrotic syndrome in the cause of kidney damage will also cause some of the body's other features of the destruction of some, that is, the disease dragged the longer the longer Will endanger the greater the ultimate function of the kidney will eventually failure to complete the function of the kidney is completely lost, is a completely can not delay the disease.

Is nephrotic syndrome harmful?

Is nephrotic syndrome harmful?

Kidney disease experts pointed out that the severity of nephrotic syndrome manifested as renal failure, uremia. In the early stages of nephrotic syndrome, if there is no effective measures to treat it, nephrotic syndrome will cause serious harm to the human body, to people's normal life and work caused a lot of inconvenience. Timely and correct treatment of the disease, so that patients get rid of nephrotic syndrome as soon as possible, with a healthy body.

When the nephrotic syndrome occurs, accompanied by nephrotic patients will occur a series of concurrent symptoms, edema, hyperlipidemia, anemia and so on. These symptoms indicate that the body resistance of patients decreased, while the body's immune regulation system has undergone tremendous changes, which will lead to abnormal expression of the body's protein, resulting in the emergence of hypoproteinemia. Nephrotic syndrome Hypoproteinemia is not only a direct impact on the body's protein needs, but also on the body there are other aspects. The human body is a complex body, its various symptoms are interrelated, mutual influence.

Due to the excretion of large amounts of proteinuria, inadequate supply of synthetic protein in the liver, leading to hypoproteinemia. The emergence of this phenomenon is a very serious nephrotic syndrome hazards. Reduce the blood protein, it will lead to decreased plasma colloid osmotic pressure, colloid osmotic pressure drop imbalance, the water will overflow within the plasma, and accumulation to the organization and body cavity, resulting in a high degree of human edema. At the same time, when the plasma water spills out, the water content in the blood decreases, and the blood volume in the active circulation is insufficient. Therefore, when the blood is reduced in water, it causes a high blood viscosity, easily forms a blood clot, Ischemia and hypoxia. The emergence of these symptoms will aggravate the process of kidney disease.

Nephrotic syndrome This disease is very high in the incidence of children in the group will have a very negative impact on the growth of children. The incidence of nephrotic syndrome is getting higher and higher, which has aroused widespread concern. Whether it can cure this disease has become one of the concerns of many patients.

Treatment for Nephrotic syndrome

Treatment for Nephrotic syndrome

Nephrotic syndrome is a relatively refractory disease, which is its repeated characteristics of the decision, and the treatment process is still relatively long. Therefore, there are many patients very anxious, there will be chaotic medical conditions, this is very wrong.

If you want a good treatment of nephrotic syndrome, we should first understand the common method of treatment in order to choose the right treatment.

First, the early treatment of edema in the disease, which is all patients will occur as a symptom. Therefore, in the treatment of the first to deal with it. Patients with severe edema and hypoalbuminemia should be bed rest. At the same time to the normal amount of high-quality protein diet, to ensure adequate calories to ensure a balanced daily nutrition. And patients with edema should be low-salt diet, if patients with hyperlipidemia should be low-fat diet.

Second, drug treatment This is the treatment of nephrotic syndrome, the most common form of treatment, but will be based on the patient's condition medication. If the patient's symptoms, should be added with a diuretic swelling, or reduce the use of urine protein drugs. Because patients with nephrotic syndrome have significant edema and serous effusion, so the simple limit of salt, water is not significant effect, the doctor can use the recommended diuretics to reduce excessive extracellular fluid. Some antihypertensive drugs can also control the role of hypertension and reduce urinary protein to varying degrees.

Third, the adrenal glucocorticoid This is a drug treatment, an important drug for the treatment of nephrotic syndrome is very effective. However, patients should be used regularly, not self-decrement or sudden withdrawal after long-term use, which may lead to poor treatment or the emergence of some serious side effects.

Patients should not be discontinued when they are treated with medication to achieve cure. If you need to disable or reduce the amount, should be carried out under the guidance of a doctor. Patients with nephrotic syndrome, the daily loss of large amounts of protein from the urine, the course of time will inevitably lead to the lack of protein in the body, then if you do not add protein, will become increasingly scarce.

To know that protein is the source of life, the body lacks protein, not only edema, and will be sick, life-threatening. The spread of kidney disease in the community to abstain from eating meat, eggs, fish without scales is unscientific. On the contrary, these patients would like to eat more protein, in particular, is rich in high quality protein foods such as milk, eggs, lean meat, chicken, fish and so on. Of course, not unlimited ingestion of protein, long-term over-ingestion of protein, not only useless, and will increase the burden on the kidneys, which lead to increased renal damage

Chinese medicine treatment

2. Chinese medicine treatment

Kidney essence from the role can be divided into kidney yin, kidney two aspects, kidney yin and kidney interdependence, mutual restraint, maintain the body's dynamic balance. Such as kidney yin partial failure can not yang, there Yin and yang hyperactivity of the lesion, that is, kidney yin deficiency, manifested as Yaoxisuanruan, five upset hot, dizziness, tinnitus, insomnia, forgetfulness, night sweats, woman spermatorrhea premature ejaculation, , Constipation, red tongue, little moss pulse fine performance. While the partial decline of kidney yang deficiency, manifested as pale or swarthy, Yaoxisuanleng, lack of energy, male impotence and premature ejaculation, female infertility Palace, edema, enuresis, diarrhea and so on. Chinese medicine is very knowledge of kidney, kidney or kidney deficiency is clear is the key. Buyyin drugs are mostly Gan Yao medicine, such as Cordyceps sinensis, Dendrobium, Polygonatum, dogwood, Chinese wolfberry fruit, female, herbal medicine, herbal medicine, herbal medicine, Sagittaria, Loranthaceae, American ginseng and so on.

3. Life maintenance of the old kidney, the body will appear the phenomenon of aging and weakness, and for the kidney itself, in particular, should pay attention to maintenance, to prevent the occurrence of kidney disease.

1, can not underestimate the common cold is a systemic disease, can make immune function, often secondary infection. According to reports, nearly 40% due to a cold caused by chronic nephritis symptoms increased, and chronic nephritis is the first chronic renal failure primary disease, it should attach great importance in daily life to prevent colds.

2, to strengthen exercise kidney disease patients due to cold weather, more reluctant to exercise throughout the winter like to stay in a warm home, or even bed rest. Doctors advise: This is a very wrong and dangerous practice, it will slow down the kidney blood flow, aggravate stasis and renal sclerosis atrophy. Nephropathy in patients with exercise-based approach to walking, sunny as far as possible to participate in outdoor sports, not suitable for outdoor activities should also be an indoor walk, do not stay in bed. For low back pain, the older people will always explain this "old man, all this." In fact, not old to have low back pain, as long as a little improvement in lifestyle and diet, you can relieve pain symptoms, and back pain that "worship." Some elderly people often back pain, can check to check to find the reason, in fact, because the mattress is too soft. Sleep, the spine can not be given appropriate support if the mattress, and the whole night in a state of improper bending, long-term sleep, the back will of course sore. Therefore, if the mattress is really soft, you can add a layer of bamboo mat above to increase the hardness, or simply change the flat bed.

The soup is characterized by "open up the blood", because the Chinese believe that only the blood will lead to soreness, so you can eat this soup to eat Open up blood, relieve pain. Do this soup wormwood to go to the pharmacy to buy, and red dates with water after the fire boil, but also a small fire and cook for 20 minutes, and then drink when the drink residue. Should be noted that the wormwood partial warm, so join the red dates must be cut to the core, or drink will get angry. In addition, if you feel the soup bitter, but also add brown sugar to taste. General drink three days a day, even drink three months, to improve the low back pain is helpful.

Treatment of Nephrotic Syndrome

First, the diet tune up

1, Cordyceps stew black-bone chicken: take 50 grams of Astragalus, 10 grams of Cordyceps sinensis, black-bone chicken 1. The black-bone chicken to the hair and internal organs, scraping clean cut, with the North Astragalus, Cordyceps together into the pot with water stew to be cooked chicken, add seasoning Yin Tang meat. Modern scientific research shows that Cordyceps sinensis is the best treatment of kidney disease in a. But not all Cordyceps have medicinal effect, the brand, the Fulin door Cordyceps sinensis and Beijing Tongrentang Cordyceps sinensis is the industry recognized the two brands. If it is to use health care, it is recommended to use Fulinmen, natural cordycepin and natural amino acid content is higher, the effect and cost-effective than good. Tong Ren Tang Cordyceps price is generally Fook Lam door 2 to 3 times. Cordyceps warm, can be taken throughout the year.

2, Seal Kidney porridge: Take the sea dog kidney 15 grams, 75 grams of rice. Kidney kidney with warm water soak for 24 hours, remove and cut open, remove the urethral layer fascia, cut into pieces, the rice Amoy net stand-by. And then take a porridge pot, into the seal kidney, the amount of water and spices, the kelp kidney cook until cooked into the rice porridge, porridge cooked food. One day. The side temperature and kidney yang effect is good.

3, Erxian stew dog: take Curculigo 10 grams, 10 grams of Faerie spleen, 250 grams of dog meat, cinnamon 6 grams, 9 grams of fennel, ginger 15 grams. Will curculigo, fairy spleen, cinnamon, fennel four drugs washed into the gauze bag Zhakou. Wash the dog meat, cut, placed in the casserole, into the medicine bag, ginger, salt, add water to stew Shoulan, remove the medicine bag, Yin Tang meat. The side of the kidney yang deficiency caused by wind cold dampness arthralgia effect is particularly good.

New progress in diagnosis and treatment of IgA nephropathy

IgA nephropathy is a group of mesangial IgA deposition characterized by mesangial proliferative glomerulonephritis, in 1968 by the French pathologist Berger first reported the disease (the disease was known as Berger's disease). It is now widely accepted that the disease is the most common manifestation of primary glomerulonephritis worldwide. Although IgA nephropathy has been considered to be "recurrent and clinically benign hematuria" in the past, IgA nephropathy is now considered to be one of the leading causes of end-stage renal disease (25-40% development of renal failure), some of which Was malignant after.

IgA nephropathy is the most common glomerulonephritis in the world, the United States and Canada account for about 2-10% of renal biopsy, Europe and Australia about 20-25%, Japan is as high as 30% or more, China is estimated to account for primary renal 20-30% of glomerulonephritis. Data from Germany and France show that IgA nephropathy in the general population incidence of 0.02%, but scholars estimate that this is just the tip of the iceberg, Singapore data show that about 2.0%. IgA nephropathy can occur at any age, but is most common in people aged 11-30 years. The ratio of males to females ranges from less than 2: 1 in Japan to as much as 6: 1 in Northern Europe and the United States. Patients of different ages, their clinical manifestations have some differences. Although primary IgA nephropathy receives the most attention, many other diseases are clinically associated with IgA nephropathy.

Table 1 IgA nephropathy classification of the main reasons

IgA nephropathy allergic purpura

Secondary cause

Liver disease: alcoholic, primary biliary, cryptogenic cirrhosis, hepatitis B;

Intestinal diseases: celiac disease, chronic ulcerative colitis, Crohn's disease

Skin diseases: psoriasis, herpes-like dermatitis

Immune rheumatic diseases: rheumatoid arthritis, Sjogren's syndrome, ankylosing spondylitis, Behcet's disease, Reiter's syndrome, immune thrombocytopenia infection: HIV infection, toxoplasmosis, leprosy

Tumor: mycosis fungoides, lung cancer, mucous secretory cancer

Diseases associated with IgA nephropathy: ANCA-associated vasculitis, diabetic nephropathy, membranous nephropathy

First, the pathology

IgA nephropathy under light microscope the most typical change is focal or diffuse mesangial cell proliferation and mesangial matrix increased. Tubulointerstitial lesions with focal tubular atrophy, inflammatory cell infiltration and interstitial fibrosis more common. IgA nephropathy glomerular lesions of light microscopy performance can vary greatly, including almost all kinds of primary glomerulonephritis pathological manifestations. Glomerular lesions from normal or minor injury to a variety of proliferation and sclerosis can be seen. Proliferation and sclerosis can be focal or diffuse, segmental or global, and can be seen in the mesangial area as well as in capillary loops, with or without necrosis, small crescent or annular body.

Whether immunofluorescence or immunohistochemical methods can detect significant deposition of IgA and C3 in the mesangial area. Further typing can be used to determine the deposition of IgA1 or IgG and / or IgM, but the deposition of C1q and C4 is rare. Active IgA nephropathy IgA can also be seen along the capillary loop deposition. At the same time there are often fibrinogen in the mesangial area, capillary loop and crescent in vivo deposition. Small blood vessel wall can be rich in C3 particles deposition, especially in patients with hypertension.

Electron microscopy showed varying degrees of mesangial cell proliferation and expansion of the mesangial matrix, the common bulk of the electron dense material in the mesangial matrix, and sometimes subendothelial mass can also be seen under the electron dense deposition. Usually basement membrane width is normal, but some patients have local thickening of the basement membrane, fracture and plaque-like changes.

Second, clinical manifestations

Clinical manifestations of IgA nephropathy are diverse, many patients have no obvious symptoms and are not aware of any problems. May be only in conventional screening or other diseases when the suspect and about 20% of IgA nephropathy patients with severe azotemia treatment. However, there are some patients may be expressed as acute lesions. IgA nephropathy mainly include the following types, the incidence of the order of:

1. Repeated gross hematuria (30-40%)

1) occurs in the upper respiratory tract infection (gastrointestinal or urinary tract infection) after a few hours to 1-2 days

2) with no more symptoms, a small number of urinary discomfort, and was diagnosed with acute cystitis

3) gross hematuria Children and adolescents (80-90%) than adults (30-40%) more common

4) has nothing to do with the severity of the disease

5) Kidney pathology is generally Lee's classification II-III level

2. Occult nephritis type (20-30%)

1) microscopic hematuria, 25% with intermittent episodes of gross hematuria

2) with or without proteinuria (+)

3) a small number of high blood pressure

4) Kidney pathology is generally Lee's classification II-III level

3. Chronic nephritis type

1) microscopic hematuria, with or without proteinuria (+ - ++)

2) often high blood pressure

3) renal function may be decreased

4) Kidney pathology is generally Lee grade II-IV

4. A large number of proteinuria or nephrotic syndrome type

1) nephrotic syndrome, with or without microscopic hematuria

2) more than a high blood pressure.

3) some patients showed nephrotic syndrome, kidney light microscope can be: minimal change and mild diffuse proliferative glomerulonephritis.

4) Kidney pathology is generally Lee grade I-IV

5. Malignant hypertension

1) malignant hypertension

2) proteinuria (+ - ++), with or without microscopic hematuria

3) often associated with renal insufficiency 4) renal pathology generally Lee grade III-IV level

6. Progressive nephritis syndrome type:

1) progressive deterioration of renal function, there is progressive oliguria

2) proteinuria (+ - ++), with or without gross hematuria

3) more than a high blood pressure, anemia

4) renal pathology is generally crescentic nephritis, Lee's classification IV-V level

Diagnosis and differential diagnosis

IgA nephropathy diagnosis must have a renal biopsy pathology, immunofluorescence or immunohistochemical results must be supported. For the vast majority of cases, the diagnosis of IgA nephropathy is not difficult. However, in some of the following cases still need to pay attention to differential diagnosis. IgA deposition in the glomerular mesangium is also associated with a variety of other diseases, IgA deposition is often accidentally discovered, its pathogenesis or clinical significance is unclear. IgA nephropathy is a common disease, so he can exist with other glomerular diseases.

1. Identification of HSPN and HSPN HSPN and IgAN are variations of the same pathological process but contribute to the systemic activation of IgA-containing immune complexes in HSP or to the local activation of IgA-containing immune complexes in IgAN Not yet determined. Purpuric nephritis is a secondary IgA nephropathy, the basic pathological features of small blood vessels inflammatory lesions, that is usually visible in the perivascular infiltration of white blood cells and nuclear debris, immunofluorescence staining confirmed involvement of the vascular wall with IgA deposition. However, when no joint pain, rash and fever, abdominal pain and other systemic symptoms, and sometimes it is indeed difficult to identify HSPN and IgAN. HSPN and IgAN have some slight differences, but not specific. Immunofluorescence changes the deposition of cellulose in HSPN. In HSPN glomeruli, many cell / fibrocytic crescents can be seen under light microscope, Glomerular necrosis or sclerosis is more common. A small number of cases can be seen in endothelial cell proliferation. Electron microscopy of HSPN can be seen subendothelial or subepithelial bulk electron dense material, and IgAN more common in the mesangial area.

2. Hypertension Renal arteriosclerosis in some patients with clinical manifestations of hypertension and renal dysfunction, renal biopsy can help distinguish between the causal relationship between the two diagnosis. Individual cases, especially immunofluorescence IgA deposition is weak, is the diagnosis of benign or malignant renal arteriosclerosis, or diagnosis of IgA nephropathy caused by renal parenchymal hypertension should be particularly careful, because further treatment and prognosis of patients with different prognosis of. Family history of hypertension, ultrasonography results will help the final diagnosis, a small number of patients even have to wait until the follow-up period of time to final diagnosis.

3. Minimal lesions For most clinical manifestations of nephrotic syndrome in patients with IgA nephropathy, leading to nephrotic syndrome is the cause of IgA nephropathy itself, but there are a small number of patients with nephrotic syndrome despite immunofluorescence IgA deposition, but the renal pathology light microscopy performance only For mild lesions, electron microscopy suggest extensive foot epithelial cell fusion, clinical response to hormone therapy, these patients should be considered the diagnosis of IgA nephropathy with minimal change, the prognosis was significantly better than pure IgA nephropathy caused by nephrotic syndrome in patients.

4. Crescentic glomerulonephritis a small number of patients with clinical manifestations of acute nephritis nephritis syndrome, pathology prompted crescentic glomerulonephritis, immunofluorescence to IgA deposition-based diagnosis should be considered type II crescentic glomerulonephritis, IgA nephropathy V Grade, anti-GBM antibodies and ANCA examination help to exclude other types of crescentic glomerulonephritis.

5 hepatitis B-associated glomerulonephritis and IgA nephropathy diagnosis can sometimes be tied, a small number of hepatitis B patients with renal pathology can be expressed as mesangial proliferative glomerulonephritis, immunofluorescence to IgA deposition, but also with hepatitis B surface antigen Or C antigen deposition in the kidney, the diagnosis should be tied for both. On the contrary some patients with IgA nephropathy, although there may be hepatitis B surface antigen or C antigen deposition in the renal pathological tissue, but if the blood markers of hepatitis B negative, the diagnosis is still IgA nephropathy.

6. Diabetic patients with diabetic nephropathy When diabetic patients with proteinuria, hematuria and the course of the disease is too short or no obvious changes in the fundus, should be considered a clear diagnosis of renal biopsy. There are three possible diagnosis of such patients, 1. Diabetic nephropathy; 2. No diabetic nephropathy, but chronic glomerulonephritis; 3. Diabetic nephropathy with chronic glomerulonephritis. Data from Korea and Hong Kong, and our own data show that diabetic patients with chronic glomerulonephritis with IgA nephropathy in the most common, accounting for more than 50%. Therefore, IgA nephropathy can be in diabetes, especially in patients with type 2 diabetes appear.

Lupus nephritis in patients with systemic lupus erythematosus, immunofluorescence results are not typical of the full house light, but mainly to IgA deposition, light microscopy showed mesangial proliferative glomerulonephritis, renal pathological diagnosis at this time should Consider IgAN, not LNI / II.

Treatment for Kidney Disease

Treatment for Kidney Disease

White / creatinine (> 3.5 for nephropathy range proteinuria).

1. Urine protein electrophoresis detection of increased urinary IgG components suggest low urinary protein selectivity. Urinary protein selectivity has no definite clinical value, is now less.

2. Hypoproteinemia: nephrotic syndrome is the second essential feature. Serum albumin less than 30g / L. Nephrotic syndrome when the liver synthesis of albumin increased, when the diet given enough protein and calories, the patient's liver synthesis of albumin per day about 22.6g, 15.6g than normal daily increase significantly. When the liver synthesis of albumin compensatory role is not enough to make up for the loss of urinary protein, will appear hypoproteinemia. Hypoalbuminemia and urinary protein excretion between the is not entirely consistent.

1), patients with nephrotic syndrome is usually negative nitrogen balance, high protein load, can be transferred to positive nitrogen balance, high protein load may be due to increased glomerular filtration protein excretion of urine protein, the plasma protein Not obvious, but at the same time taking blood angiotensin converting enzyme inhibitor, can prevent urinary protein excretion, serum albumin concentration can be significantly increased.

2), it is noteworthy that, hypoalbuminemia, the combination of drugs and albumin will be reduced, free drug concentration in the blood, may increase the toxicity of drugs.

3), nephrotic syndrome, a variety of plasma protein components can change, α2 and β globulin increased, α1 globulin and more normal. IgG, IgA, IgM, IgE levels were normal or increased, fibrinogen, coagulation factors Ⅴ, Ⅶ, Ⅷ, Ⅹ can be elevated, may be associated with increased liver synthesis, with increased platelet count, anticoagulation Blood enzyme Ⅲ (heparin-related factors) decreased, C protein and S protein concentration more than normal or increased, but the activity decreased. This will contribute to the occurrence of hypercoagulable state. Urinary fibrin degradation products (FDP) increased, reflecting the glomerular permeability changes. In short, blood coagulation and agglutination of a variety of pre-factors are increased, and anti-coagulation and fibrinolysis mechanism of damage. Due to the combined effects of hypercholesterolemia and hyperfibrinogenemia, plasma viscosity increases and spontaneous thrombosis occurs when the vascular endothelium is damaged.

4). In addition, the transport protein is also reduced, such as carrying important metal ions (copper, iron, zinc) protein decreased, and important hormones (thyroxine, cortisol, prostaglandin) and active 25- (OH) D3 Of the protein also decreased, which can lead to secondary hyperparathyroidism, calcium and phosphorus metabolism disorders, lead to renal bone disease. Continuous reduction of transferrin, the glucocorticoid in the treatment of patients with free and combined hormone ratio changes, leading to the drug metabolism and efficacy change.

3. Hyperlipidemia The total cholesterol, triglyceride significantly increased, low density lipoprotein (LDH), very low density lipoprotein (VLDH) levels. Hyperlipidemia and hypoalbuminemia, LDL / HLDL only in serum albumin less than 10 ~ 20g / L when increased. High-density lipoprotein (HDL) normal or decreased. LDL / HDL ratio increased, the occurrence of atherosclerotic complications of increased risk, hyperlipidemia and thrombosis and progressive glomerulosclerosis. Patients may have lipid urine, urine refraction of fat body appears, may be cholesterol-containing epithelial cells or fat tube type.

4. edema of the most noticeable symptoms of patients is gradually aggravated systemic edema, the initial morning eyelid, facial, ankle edema; with the development of edema affected the body and the emergence of pleural effusion, ascites, pericardial effusion, mediastinal Fluid, scrotal or labia edema, pulmonary edema can also occur. Severe eyes can not open, head and neck thicker, the skin can be waxy pale, combined with the presence of chest and ascites, it appears obvious difficulty breathing, can not be supine only sitting position. If there is skin damage, the organization of fluid overflow and difficult to stop. Edema and postural relations, such as the emergence of postural edema, should not be suspected and venous thrombosis. The severity of edema is generally associated with the degree of hypoalbuminemia. Is generally believed that edema is caused by a large number of proteinuria plasma protein (especially albumin) decreased plasma colloid osmotic pressure decreased intravascular water to the tissue gap caused by the move. Another that the intrinsic edema and primary renal sodium and water retention, the possible factors are:

① glomerular filtration rate decreased;

② tubular reabsorption increased;

③ distal tubule on plasma atrial natriuretic peptide (ANP) decreased ability to respond.

Immune System Reboots During Sleep

　　Immune System Reboots During Sleep
　　Blood samples were taken from 14 healthy young men, average age 25, when they slept through the night and again when they stayed awake all night. The samples were analyzed for levels of T-cells, which are white blood cells that are the foundation of the immune system.
　　When the participants got a full night's sleep, levels of all types of T-cells fell within three hours of falling asleep. But T-cell levels stayed high when the volunteers stayed awake all night.
　　It's not clear where T-cells went when they left the bloodstream during sleep. But, previous research suggests they may accumulate in lymph nodes, according to the authors of the study published recently in the American Journal of Physiology -- Regulatory, Integrative and Comparative Physiology.
　　The rapid fall in T-cell levels in the blood during sleep shows "that even one night without sleep affects the adaptive immune system," study first author Luciana Besedovsky said in a journal news release. "This might be one reason why regular sleep is so important for general health."
　　Besedovsky is a researcher in the Department of Medical Psychology and Behavioral Neurobiology at the University of Tubingen in Germany.

Why Can't I Breathe?

　　Why Can't I Breathe?
　　It's not a surprise to find yourself short of breath after a workout. But are you out of air when you're at rest, or even lying down? If so, it might be a sign of a larger problem. You need to get it checked out by your doctor right away.
　　Shortness of breath is a symptom of a lot of medical conditions. Watch out for other issues that may go along with your airflow problem.
　　Allergies
　　Your breathing trouble could be an allergy to a food, pet, or something in the air. Your immune system -- the body's defense against germs -- treats those things like a foreign invader that needs to be fought off.
　　Besides shortness of breath, you might have:
　　Vomiting
　　Hives or rash
　　Coughing, sneezing, or runny nose
　　Watery eyes
　　Tightness in the throat
　　Trouble swallowing or swelling of your tongue
　　Dizziness
　　Fatigue
　　Some common foods that some people are allergic to are eggs, milk, nuts, shellfish, and wheat. Things in the air that can set off your allergies are dust, pollen, and pet dander -- tiny pieces of skin that are shed by cats, dogs, and other animals.
　　Your doctor can give you tests that pinpoint the triggers for your allergies. Medications, such as antihistamines, can help relieve many symptoms. Your doctor may also recommend immunotherapy, a long-term treatment plan that involves regular injections.
　　Asthma
　　It might feel like someone is sitting on your chest or you can't get enough air in or out. You take short breaths to try to get as much in.
　　Asthma is one of the most common lung diseases. It can be triggered by something you're allergic to, like pollen, or from an irritant in the air, like smoke. Stress, exercise, or even a change in the weather can set it off.
　　In addition to shortness of breath, it can cause:
　　Coughing
　　Tightness in the chest
　　Wheezing
　　To keep it under control, work with your doctor to create a treatment plan. First, avoid all triggers except exercise, which is important for your overall health.
　　You can try two kinds of medicines. One is for long-term control and the other is for quick relief.
　　Atrial Fibrillation
　　Your heart works hard for you your whole life. But sometimes its rhythm gets off-kilter. When it skips a beat or flutters in an unusual way, it's known as atrial fibrillation (AFib). The upper chambers of your heart quiver, and it can become less effective at pumping blood. This can lead to blood clots, stroke, and heart failure.
　　When you have AFib, you'll notice some other symptoms besides shortness of breath.
　　Fatigue
　　Rapid or irregular heartbeat
　　Dizziness
　　Weakness
　　Anxiety
　　Faintness
　　Sweating
　　Chest pains
　　Doctors can treat your AFib with medications, but you can also keep it in check by some lifestyle changes, such as drinking less coffee.
　　Chronic Obstructive Pulmonary Disease (COPD)
　　It's a type of lung disease that mainly involves two conditions: long-term bronchitis and emphysema. It's generally caused by smoking.
　　Over time, your lung tissue gets damaged, and you find it harder to draw air in and out of your lungs.
　　Some other signs of COPD are:
　　Coughing
　　Frequent respiratory infections
　　Blue lips or fingernails
　　Fatigue
　　Too much phlegm or mucus
　　Wheezing
　　COPD can be managed with medication, but there's no cure, and it gets worse over time. A change in lifestyle, including exercise and eating right, can help. You may need doses of extra oxygen from a tank or another device. Your doctor might recommend surgery to repair your damaged lungs.
　　Is It Because I Quit Smoking?
　　If you've been smoking for a while, it shouldn't be a surprise if you can't breathe as well. Of the many health problems that come with tobacco, lung disease is at the top.
　　But you may not realize that when you stop lighting up, you can have short stints where you can't catch your breath.
　　As you smoke, you damage your lungs. It can take a while for them to heal once you've stopped. Aside from trouble breathing, you can have:
　　Craving for cigarettes or nicotine
　　Intense hunger
　　Coughing
　　Headaches
　　Trouble concentrating
　　Constipation
　　Fatigue
　　Sore throat
　　Trouble sleeping
　　After you put out your last cigarette, your ability to breathe normally should return in 1 to 9 months. It depends on how long and heavily you smoked.
　　What Can I Do About Shortness of Breath?
　　Don't ignore your breathing troubles or put off getting help. Your body is trying to tell you something important. Get in touch with your doctor to find the source of the problem and learn how to get relief. Once you've got a diagnosis, you'll be one step closer to breathing easier.

What is diabetic nephropathy

What is diabetic nephropathy

What is diabetic nephropathy, how to control? Diabetic nephropathy is commonly referred to as diabetic microangiopathy caused by diabetes - diabetic glomerulosclerosis, diabetic renal arteriosclerosis and pyelonephritis. The main feature of the lesion is glomerular (capillary plexus within the kidneys) localized or diffuse sclerosis. Glomerular sclerosis is mainly caused by long-term high blood sugar to the glomerular basement membrane on the glomerular glycoprotein and glycosylated protein increased basement membrane thickening, increased permeability, and hypertension, autoimmune, genetic, etc. factor. Thus, the occurrence and development of diabetic nephropathy and diabetes control is good or bad to the length of the course of disease is closely related to clinical research found that effective control of diabetes can stop or delay the occurrence of diabetic nephropathy. At present, diabetic nephropathy is still one of the most serious complications of diabetes, diabetes is one of the most important causes of death.

 According to clinical manifestations of diabetic nephropathy can be divided into: common in patients with a history of more than 10 years, is the main cause of death in type 1 diabetes is divided into five: Ⅰ: increased glomerular filtration rate and renal volume increased to feature. This initial lesion is consistent with hyperglycemia, but is reversible and can be restored by insulin therapy, but does not necessarily completely restore normal glomerular hypertrophy leading to increased filtration.

Ⅱ period: the urinary albumin excretion rate is normal but the glomerular structure has been changed. This period of urinary albumin excretion rate (UAE) normal (<20μg / min or <30mg / 24h), UAE increased after exercise rest after rest. Glomerular capillary basement membrane (GBM) thickening and increased mesangial matrix, GFR more than normal and consistent with the blood glucose levels, GFR> 150mL / min patients with glycated hemoglobin often > 9.5%. GFR> 150mL / min and UAE> 30μg / min after the patients more likely to develop clinical diabetic nephropathy. Diabetic renal damage in patients with stage Ⅰ, Ⅱ more normal blood pressure. Ⅰ, Ⅱ GFR patients increased, UAE normal, so the two can not be called diabetic nephropathy protein filtration stage Ⅲ: also known as early diabetic nephropathy. Urinary albumin excretion rate of 20 ~ 200μg / min, the patient's blood pressure increased slightly, began to appear abandoned glomerular. Ⅳ period: clinical diabetic nephropathy or dominant diabetic nephropathy. This phase is characterized by massive albuminuria (greater than 3.5 grams per day), edema and hypertension. Diabetic nephropathy is more serious edema, poor response to diuretics. Stage V: end-stage renal failure. Diabetic patients once the persistent urinary protein development for clinical diabetic nephropathy, due to extensive glomerular basement membrane thickening, glomerular capillary luminal stenosis and more glomerular waste, renal filtration function decreased, Leading to renal failure. The progress of diabetic nephropathy in each patient is different, and some patients with mild proteinuria sustainable for many years, while renal function has remained normal. Some patients with minimal proteinuria, but soon developed into severe proteinuria (≥ 3 to 5 g / day) such patients with poor prognosis.

 Treatment of diabetic nephropathy principles: ① strict control of blood sugar, blood sugar as close to normal levels as possible to prevent and delay the occurrence of diabetic nephropathy; ② delay the rate of renal dysfunction; ③ dialysis treatment and kidney transplantation. Prevention and treatment of diabetic nephropathy: 1. Strict control of blood sugar, before the emergence of clinical diabetic nephropathy, that is, early in the diabetes, insulin pump or subcutaneous insulin injections to strictly control diabetes, so that blood sugar remained normal, can delay or even prevent diabetes The occurrence and development of nephropathy, reduce the increased glomerular filtration rate and improve microalbuminuria. Other complications are also beneficial. According to the DCCT study, T1DM with intensive insulin therapy, the incidence of diabetic nephropathy decreased by 35 %% - 55 %%. Has been developed to clinical diabetic nephropathy, there are significant proteinuria, blood glucose control to help the development of its disease smaller. After the emergence of clinical diabetic nephropathy, hypoglycemic drugs should generally use insulin. 2. Control of high blood pressure, high blood pressure will promote the development of renal failure, effective antihypertensive treatment can slow down the rate of glomerular filtration rate, reduce urinary albumin excretion. Angiotensin converting enzyme inhibitors or angiotensin Ⅱ receptor antagonists can be used as the drug of choice, often in combination with other antihypertensive drugs. Other antihypertensive agents such as calcium antagonists, diuretics, beta-blockers, methyldopa, clonidine, etc. are also effective. Diabetic patients with blood pressure ≥ 130 / 80mmHg should use antihypertensive drugs, should be controlled at 130 / / 80mmHg the following. Treatment with antihypertensive drugs, the relatively healthy glomerular glomerular capillary pressure drop and continue to survive, but has been completely blocked the glomerular obstruction, water can not be filtered, the protein can not leak. It was observed that blood pressure decreased from 160 / 95mmHg to 135/85-mmHg, urinary protein excretion was significantly reduced glomerular filtration rate decreased from lml / / min · month to 0.35ml / / min · month . Diabetic nephropathy patients also significantly longer survival, antihypertensive treatment 10 years before the cumulative mortality rate of 50 %% - 70 %%, after treatment down to 18 %%. Antihypertensive therapy is also beneficial for diabetic retinopathy. 3. Diabetic nephropathy has occurred in patients with restricted protein intake, an appropriate diet to reduce the amount of protein (0.8 / kg · d) can reduce glomerular pressure, reduce high filtration and reduce proteinuria. On the contrary, to high-protein diet will aggravate glomerular histological lesions. Renal dysfunction has occurred should limit the intake of protein, and should eat essential amino acids with high protein. 4. Patients with advanced dialysis and renal transplantation can be implemented, once the emergence of renal failure, dialysis and kidney transplantation is the only effective way. Kidney transplantation is the best way to treat diabetes uremia, better than dialysis. Patients> 65 years old are poorly transplanted. 5. Attention to personal hygiene to prevent the occurrence of urinary tract infections. 6. Avoid the use of drugs harmful to the kidneys.

Renal parenchymal hypertension

Renal parenchymal hypertension

Renal parenchymal hypertension diagnosis depends on: (1) history of renal parenchymal disease; proteinuria, hematuria and renal dysfunction occurred before or at the same time in hypertension; (2) physical examination often have anemia appearance, kidney mass Serum creatinine, uric acid, blood glucose, blood lipid determination; 24-hour urinary protein or urinary albumin / creatinine ratio (ACR (serum creatinine, urinary albumin, creatinine); ), 12h urinary sediment examination, such as proteinuria, hematuria and urinary white blood cells increased, you need to further the middle of urine culture, urine protein electrophoresis, urine phase contrast microscopy, clear urine protein, red blood cells and exclude infection; Kidney size and shape, and whether the tumor; found kidney volume and shape abnormalities, or found in the tumor, you need to do further renal CT / MRI to diagnose and check the cause; fundus examination; if necessary, the condition of the hospital line kidney Puncture and pathology, which is the diagnosis of renal parenchymal disease of the "gold standard." (4) renal hypertension and renal hypertension need to be caused by renal damage and pregnancy-induced hypertension phase identification, the former often preceded the occurrence of renal disease or hypertension at the same time with it; high blood pressure and difficult to control, easy to progress to Malignant hypertension; proteinuria / hematuria occurred early, severe degree, impaired renal function significantly. Pregnancy within 20 weeks of hypertension with proteinuria or hematuria, and prone to pre-eclampsia or eclampsia, there are still high blood pressure after childbirth, renal parenchymal hypertension. Renal parenchymal hypertension treatment should include low-salt diet (daily <6g); a large number of proteinuria and renal insufficiency, should choose a high intake of high-value protein, and limited to 0.3-0.6g / kg / d; In patients with proteinuria should be preferred ACEI or ARB as antihypertensive drugs; long-acting calcium channel blockers, diuretics, β-blockers, antihypertensive drugs, Α blockers can be used as a combination therapy drugs; such as glomerular filtration rate <30ml / min or a large number of proteinuria, thiazide diuretics ineffective, loop diuretics should be used in the treatment of about 90% of the kidney Essential hypertension is due to Shuinazhuliu and blood volume expansion due. When the renal parenchymal lesions make the kidneys lose excretion diet contains the right amount (not excessive) water, salt, it will cause water, sodium retention in the body, thereby causing excessive blood volume caused by high blood pressure. This mechanism occurs as long as there is mild renal insufficiency. Plasma renin and angiotensin II (A II) levels are usually low in these patients. its

Hypertension can limit the water, salt intake or by dialysis to remove excess water, salt to achieve the purpose of lowering blood pressure. Whether unilateral or bilateral renal parenchymal disorders, almost every kidney disease can cause high blood pressure. Usually glomerulonephritis, lupus nephritis, polycystic kidney disease, congenital renal hypoplasia and other diseases, if the disease is more extensive and associated with vascular disease or renal ischemia more extensive, often accompanied by high blood pressure. For example, diffuse proliferative glomerulonephritis often due to extensive disease, severe renal ischemia, hypertension is very common; the other hand, minimal change, focal proliferative nephritis rarely hypertension. Renal tuberculosis, kidney stones, renal amyloidosis, hydronephrosis, pure pyelonephritis, renal medullary cyst disease and other major manifestations of interstitial damage of renal tubular lesions produce less chance of hypertension. However, these diseases once developed to affect glomerular function often appear high blood pressure. Therefore, the incidence of renal parenchymal hypertension and glomerular function status is closely related. Glomerular dysfunction, blood pressure tends to rise, end-stage renal failure, the incidence of hypertension up to 83%.