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%.

Diabetic nephropathy in the treatment of diabetic nephropathy prescription

Diabetic nephropathy in the treatment of diabetic nephropathy prescription

(1) 60 grams of dried corn, potassium chloride 1 gram. Corn must be washed with water, and then add 500 ml of water, fry to 250 ml, morning and evening 2 sub-service. At the same time, serving potassium chloride 1 g, 3 times a day. Applicable to various types of diabetic nephropathy. Daily diet need to pay attention to, regular exercise to improve immunity. Diabetic nephropathy in the prescription

(2) live carp 2 (each about 50 grams), Burnet 15 to 30 grams, 9 to 15 grams of fresh rhubarb. Wash the fish, boiled with the above traditional Chinese medicine, half an hour before going to bed to eat fish soup. 1 day, 3 to 5 for a course of treatment. Applicable to various types of diabetic nephropathy. Stay up early to get up early can not stay up late, you can avoid sub-health, not easy to get sick. Treatment of diabetic nephropathy prescription

(3) Purple single head of garlic, castor seed 60 to 70 tablets. Will be two drug skin and shell off, with a mash (not placed too long), divided into two equal parts, respectively, coating the soles of the feet Yongquan, topical cellophane covered with a bandage tie, coating 1 week. Such as the effect is not good, then the top coating 7 days. Forbidden oral. Applicable to various types of diabetic nephropathy. Water is easily absorbed through the cell membrane by the body, so that human organs in the lactate dehydrogenase activity increased, thus effectively improve the body's resistance to disease and immunity.

(4) a centipede, a raw egg. The centipede head to the end of drying for the end of the egg from the pre-knock knocked into the egg inside the mixing, external wet paper and loess package simmer cooked, stripped of eggs to eat, eat a day, 7 days for a course of treatment. Such as urinary protein is not retired, and then served a few courses. Two courses in the middle separated by 3 days. Eggs should be included in the total daily intake of eggs during the heat. This side with hyperlipidemia should not be taken. Ill need more maintenance is not easy, often exercise to improve the immune system.

(5) black sesame seeds, walnuts, 500 grams each for a material. Two things are sent to the next warm water, each 10 grams, after serving service jujube 3, 3 times a day. After serving a material for a course of treatment. Medication should be regularly checked during urine routine, if the protein disappeared, the first 4 months can be separated by 1 to 2 days to take 1, after serving service jujube 3. This applies to all types of diabetic nephropathy.

(6) Astragalus, corn, glutinous rice root 30 grams, fried glutinous rice 10 grams. Jianshui tea, fractional service. 1 day, do not interrupt, even for 3 months. Medication should be regularly checked during the urine routine, if the disappearance of urinary protein, the first 4 months can be separated by l ~ 2 days a service. Less protein in urine for six months, the amount of service for more than a year. For Qi-diabetic nephropathy, Zheng Jian Shenpi fatigue, pale complexion minimalist, urinary protein in the course of time.

(7) Kochia scoparia 15 grams, leech powder 3 to 5 grams (into the capsule), yam 30 grams, 15 grams of dodder, Astragalus 30 grams, 18 grams of Poria, raspberry 15 grams. In addition to leech powder, the more than 6 herbs decoction 2 times, concoction 300 ml, sooner or later divided into fasting. Leeches powder into the capsule, 2 times delivery service. Applicable to kidney deficiency type diabetic nephropathy, Zheng Jian back pain limb soft, Shenpi fatigue, urine protein. Attention to eating habits, not overeating on the body is not good, easy to get gastrointestinal diseases.

(8) Astragalus 45 grams, 25 grams of red peony, Chuanxiong, Angelica, Gallus gallus domesticus, 15 grams of each herb, peach kernel, safflower, rhubarb 6 grams, 30 grams of Loranthaceae. For blood stasis type diabetic nephropathy, Zheng Jian urinary protein, fatigue, pale complexion and so on