Interstitial nephritis diet need to pay attention to what

Interstitial nephritis diet attention to what patients should pay attention to the problem, we treat diet is very important for our health and diet for patients, even more important,patients must pay attention to diet in the treatment process,some foods will aggravatethe condition of the patient, the drug's effectiveness.
Interstitial nephritis diet taboo: taboo irritating foods: wine, tea, coffee: a variety ofcondiments such as onions, ginger, garlic, curry, mustard, pepper.
Interstitial nephritis food taboos: should not eat spinach, bamboo shoots, AmaranthusLevin and beans and soy products, animal offal, and concentrated chicken soup, broth, etc..
Interstitial nephritis food taboos: fast fried food. Forbidden to eat food containingnucleoprotein.
The mechanism of infection caused by interstitial nephritis is not yet entirely clear, someof these pathogens can directly invade the kidney, the cells involved in stromal reactionby the production of anti-invasive pathogens, antibodies, cells and phagocytic cells. Thebacteria invade the kidney release of endotoxin or exotoxin directly damaged tissue.
Drug-induced acute interstitial nephritis is usually caused by an allergic reaction, and therelationship of the direct toxic effects not only due to acute interstitial nephritis occurred ina small number of patients in the medication, dose, kidney damage is often accompanied by allergic systemic manifestations (fever, rash, eosinophilia, arthralgia),re-exposure to the same drug or similar drugs may still react, some of the causative drugantibodies in the loop, while a number of humoral or cellular immune responses mediated by the evidence.

Purpura nephritis five complications

1 Rash.
The rash is a skin lesion. The change from a simple skin color to the skin surface uplift or blisters, etc. There are a variety of manifestations. Performance, often for the first onset of purpura of varying sizes, higher than the surface of the skin was purple, pressure does not fade and can be integrated into the film, or was a herpes-like, urticarial or more erythema multiforme can be associated with peripheral edema.
Can occur even in severe ulceration and necrosis. The purpura common extensor surfaces of the limbs and buttocks, lower limb and ankle, knee and other joints more symmetrically batches, easy recurrent.
2 Joint symptoms.
Purpura nephritis in patients with joint symptoms, the majority of migratory polyarthralgia characterized. Commonly involved joints are the knee, ankle and hand. The symptoms subsided more than a few days, not left to joint deformity. Some children of the relevant section of swelling, pain, mostly involving large joints, such as knee, ankle, wrist, elbow and other small joints are not affected. Single, multiple or were migratory. Joint swelling, pain, pain during activity increase, the local is often accompanied by micro-hot, heavy burning sensation. Joint symptoms subsided without sequelae.
3 Gastrointestinal symptoms.
Purpura nephritis in patients with gastrointestinal manifestations most commonly abdominal pain, mainly umbilical and abdominal colic. May be associated with nausea, vomiting and bloody diarrhea, occasional vomiting. Children purpura nephritis can sometimes be complicated by intussusception, intestinal obstruction and intestinal perforation.
4 High blood pressure.
Purpura nephritis induced hypertension accounts for about 20% to 40% of patients with hypertension, blood pressure is generally mild to moderate increased cases of individual patients with purpura nephritis hypertensive encephalopathy. Also found that high blood pressure often with urinary abnormalities, but the majority of patients with purpura nephritis recovered rapidly.
5 Urinary tract symptoms.
The majority of children with purpura nephritis performance of urine, small amount of protein and microscopic red blood cells, sometimes see a tube type, but also had gross hematuria. Generally good prognosis, even showed a rapidly progressive glomerulonephritis after development of acute renal failure and poor prognosis. Some children have proteinuria, hematuria, edema, hypertension, hypoalbuminemia and hypercholesterolemia such as nephrotic syndrome.

Purpura nephritis ate purpura nephritis

Purpura nephritis to eat what is now many patients are more concerned about the problem, because this disease is very common, and it is more difficult to cure, and understanding these will heal a lot of convenience. The disease is mostly caused by allergy patients in peacetime must pay attention to some allergic.
Determined from the cause of the disease, Henoch-Schonlein purpura nephritis patients is neither strictly control the protein intake, but also not too much emphasis on high-protein diet, the daily protein intake of 1g / kg body weight is appropriate , and high-quality protein-based. The adult daily intake of about 60 grams of high biological protein-based, such as eggs, lean meat, fresh milk. Henoch-Schonlein purpura nephritis patients without edema or hypertension do not have to salt restriction. Limit salt intake in patients with edema and hypertension, general daily control at 2-3 grams of salt, oliguria, elevated serum potassium should be limited to the potassium salt intake. Henoch-Schonlein purpura nephritis in patients with oliguria, edema does not need to control water intake, edema patients to master the water intake should be based on the extent of the urine and edema, in general, if edema, in addition to eating outside, the water intake is best limited to 500-400ml / day more appropriate.
The experts pointed out that the purpura nephritis patients should be fasting allergy foods, fried foods, aquatic products (such as shrimp, crab), spicy foods (such as pepper, garlic, raw onions, cilantro), dog, horse, donkey and so on. Mainly in low-salt diet, light foods rich in vitamins, different types of patients may be appropriate to add a little seasoning. Purpura nephritis clinical points of the actual situation, to take a balanced treatment system "of" natural immune system, symptomatic treatment with diet to restore, you can often receive a more desirable effect. Purpura nephritis, the diet should be to master the principle of two aspects: on the one hand, to prevent further allergic; the one hand, and kidneys, kidney, reducing the extent of damage to the kidneys. Patients with diet are advised to eat a nutrient-rich, easy-to-digest foods, eat more fresh vegetables and fruits, eat seafood fat objects, Xin dry the goods, as well as fish, shrimp, crab, milk and other food heterosexual protein, quit alcohol.
Purpura nephritis, the diet should be light, nutritious and digestible and absorbed, to avoid the practice of some improper diet, avoid fatty, each meal should not have fed, to avoid increasing the burden on the stomach, induce or exacerbate gastrointestinal bleeding. Purpura nephritis diet diet should be finished, minimize the use of coarse food or crude fiber and more food, because the coarse food or crude fiber wear the gastrointestinal mucosa, induce or aggravate gastrointestinal bleeding, you can eat melon, cabbage leaves. Purpura nephritis diet is neither strict control of protein intake, but also not too far to the emphasis on high-protein diet, plasma proteins continues to lower allows the resilience to land, prone to infection, edema repeat, worse, high-protein diet can cause glomerular hyperfiltration, a long time to promote glomerular sclerosis.The daily protein intake of 1g / kg body weight is appropriate and high quality protein-based. Proteins could be appropriate use of adult daily intake of about 60 grams of high biological protein-based milk.
Is now clear purpura nephritis should not eat what? Patients when the disease is found to be timely given medical treatment to prevent disease progression, but must pay attention to the prognosis of nursing work.

Purpura nephritis treatment

Light cases, only symptomatic treatment, most cases have fully recovered. Critically ill patients, such as acute nephritic syndrome, nephrotic syndrome and rapidly progressivenephritic syndrome requiring aggressive treatment, including the use of adrenalcorticosteroids, immunosuppressive agents, anticoagulant therapy and plasmapheresis.
Purpura nephritis treatment of specific measures:
① acute phase patients should pay attention to the rest, severe should be bed rest;
② diet care, according to the condition varies, you can refer to the book of acutenephritis, nephrotic syndrome and renal failure;
③ discovery and removal of allergens, the existence of foci, should be treated with antibiotics, stop taking it and contact may be allergens in food and drugs;
④ adrenal cortex hormone application, can ease joint pain and reduce soft tissueedema, suitable for severe joint pain and abdominal pain patients and nephrotic syndrome, and the former can be used 1 ~~ 2mg/kg of prednisone daily for 7 to 14 days to the latter prednisone daily 1 ~ 2mg/kg, plus service cyclophosphamide 2 mg / kg, a course of treatment in about 6 to 12 months.

Diet food taboos of lupus nephritis

Diet food taboos, diet is an important part of Chinese medicine treatment of diseases, health and fitness. Disease do not pay attention to diet can aggravate the condition, do not pay attention to diet when taking the drug, the drug may occur with the food of some physical or chemical change, such as precipitation, and decomposition, allows drugs of lower potency, and even increase the toxicity of some adverse reactions, and made it worse or life threatening. One taboo for certain diseases to certain foods, such as medicine cold and heat, warm and cool food attributes cool and cold and heat, so the emphasis on dietary taboo in traditional Chinese medicine treatment. The Neijing said heart disease avoid temperature food, lung disease avoid Cold Food for the nature of the food, liver ban Xin, heart disease ban salt, liver ban acid, kidney ban Gan, lung forbidden bitter. Refers to the smell of food. Food taboos of modern medicine is based on the diseased organs and pathological and clinical characteristics. Taking medications need taboo to certain foods, food taboos of traditional Chinese medicine more if aspartic avoid carp; the Atractylodes avoid Taoli; turtle bogey amaranth; honey avoid onions and garlic; the Nepeta avoid fish, turtles, and so on. Lupus erythematosus treatment and rehabilitation process, there are certain foods can trigger or aggravate lupus disease, as follows:
Seafood (1), commonly known as fat objects. Some lupus patients after the consumption of seafood allergy (in patients with systemic lupus erythematosus most highly allergic) to induce or aggravate the condition.
(2), mutton, dog meat, venison, longan, sex hot, lupus patients showed a yin deficiency heat phenomenon, and enables patients with heat symptoms get worse after eating.
(3) parsley, celery long food cause photosensitivity, so that patients with facial erythema skin lesions, it is unfit for human consumption.
(4) spicy food, such as pepper, raw onions, raw garlic, etc. can increase the heat phenomenon in patients unfit for human consumption.
(5) the absolute prohibition of smoking, drinking.
Actually lupus erythematosus diet is very complex, and also varies from person to person. Listed above these taboos is only relative in general, individual differences, individual problems should be individual treat. To grasp the principle is neither unworthy, nor unscrupulous patients according to their own personal experience to properly grasp.
Lupus rehabilitation soup comprehensive regulation of the human endocrine system, and effectively restore the function of internal organs and blood of yin and yang, effective prevention of disease recurrence and rebound, leaving the overall function be restored leaving this disease completely recovered. Endorsed 0 | Comments

What are the dietary requirements of purpura nephritis

What are the dietary requirements of purpura nephritis, many patients in their daily livesare not serious control. Because some patients in their daily lives, there are some poor eating habits, in patients with these adverse effects, use some food, increase thepatient's condition and reduce the patient's treatment, the patient's condition can not be effectively controlled. Purpura nephritis how to arrange the diet. Following on from our experts tell you about purpura nephritis diet.
Purpura nephritis, the diet requires an intake of water
Henoch-Schonlein purpura nephritis in patients with oliguria, edema does not need tocontrol water intake, edema patients to master the water intake should be based on theextent of the urine and edema, in general, if edema, in addition to eating outside, thewater intake is best limited to 500-800ml / day more appropriate. Suffering from urinary tract infections, in order to avoid and reduce bacteria in the urinary tract to stay andbreed, patients should drink plenty of water, ground urination, often to flush the bladder and urethra.
Purpura nephritis, dietary requirements, the requirements of the salt
Henoch-Schonlein purpura nephritis patients without edema or hypertension do not haveto salt restriction. Limit salt intake in patients with edema and hypertension, not limited tosalt may aggravate sodium retention and edema are hard to dismiss, causing high blood pressure. General every day, control salt 2-3 grams, oliguria, elevated serum potassiumshould limit the potassium salt intake.
Purpura nephritis, dietary requirements, taboo food
Allergy foods, fried foods, aquatic products such as shrimp, crab, spicy foods such aschili, garlic, raw onions, parsley, dog, horse, donkey. Mainly in low-salt diet, light foods rich in vitamins, different types of patients may be appropriate to add a little seasoning,such as a small amount of sesame oil, MSG and other.What are the dietary requirements of purpura nephritis, many patients in their daily livesare not serious control. Because some patients in their daily lives, there are some poor eating habits, in patients with these adverse effects, use some food, increase thepatient's condition and reduce the patient's treatment, the patient's condition can not be effectively controlled. Purpura nephritis how to arrange the diet. Following on from our experts tell you about purpura nephritis diet.
Purpura nephritis, the diet requires an intake of water
Henoch-Schonlein purpura nephritis in patients with oliguria, edema does not need tocontrol water intake, edema patients to master the water intake should be based on theextent of the urine and edema, in general, if edema, in addition to eating outside, thewater intake is best limited to 500-800ml / day more appropriate. Suffering from urinary tract infections, in order to avoid and reduce bacteria in the urinary tract to stay andbreed, patients should drink plenty of water, ground urination, often to flush the bladder and urethra.
Purpura nephritis, dietary requirements, the requirements of the salt
Henoch-Schonlein purpura nephritis patients without edema or hypertension do not haveto salt restriction. Limit salt intake in patients with edema and hypertension, not limited tosalt may aggravate sodium retention and edema are hard to dismiss, causing high blood pressure. General every day, control salt 2-3 grams, oliguria, elevated serum potassiumshould limit the potassium salt intake.
Purpura nephritis, dietary requirements, taboo food
Allergy foods, fried foods, aquatic products such as shrimp, crab, spicy foods such aschili, garlic, raw onions, parsley, dog, horse, donkey. Mainly in low-salt diet, light foods rich in vitamins, different types of patients may be appropriate to add a little seasoning,such as a small amount of sesame oil, MSG and other.What are the dietary requirements of purpura nephritis, many patients in their daily livesare not serious control. Because some patients in their daily lives, there are some poor eating habits, in patients with these adverse effects, use some food, increase thepatient's condition and reduce the patient's treatment, the patient's condition can not be effectively controlled. Purpura nephritis how to arrange the diet. Following on from our experts tell you about purpura nephritis diet.
Purpura nephritis, the diet requires an intake of water
Henoch-Schonlein purpura nephritis in patients with oliguria, edema does not need tocontrol water intake, edema patients to master the water intake should be based on theextent of the urine and edema, in general, if edema, in addition to eating outside, thewater intake is best limited to 500-800ml / day more appropriate. Suffering from urinary tract infections, in order to avoid and reduce bacteria in the urinary tract to stay andbreed, patients should drink plenty of water, ground urination, often to flush the bladder and urethra.
Purpura nephritis, dietary requirements, the requirements of the salt
Henoch-Schonlein purpura nephritis patients without edema or hypertension do not haveto salt restriction. Limit salt intake in patients with edema and hypertension, not limited tosalt may aggravate sodium retention and edema are hard to dismiss, causing high blood pressure. General every day, control salt 2-3 grams, oliguria, elevated serum potassiumshould limit the potassium salt intake.
Purpura nephritis, dietary requirements, taboo food
Allergy foods, fried foods, aquatic products such as shrimp, crab, spicy foods such aschili, garlic, raw onions, parsley, dog, horse, donkey. Mainly in low-salt diet, light foods rich in vitamins, different types of patients may be appropriate to add a little seasoning,such as a small amount of sesame oil, MSG and other.phritis, many patients in their daily livesare not serious control. Because some patients in their daily lives, there are some poor eating habits, in patients with these adverse effects, use some food, increase thepatient's condition and reduce the patient's treatment, the patient's condition can not be effectively controlled. Purpura nephritis how to arrange the diet. Following on from our experts tell you about purpura nephritis diet.
Purpura nephritis, the diet requires an intake of water
Henoch-Schonlein purpura nephritis in patients with oliguria, edema does not need tocontrol water intake, edema patients to master the water intake should be based on theextent of the urine and edema, in general, if edema, in addition to eating outside, thewater intake is best limited to 500-800ml / day more appropriate. Suffering from urinary tract infections, in order to avoid and reduce bacteria in the urinary tract to stay andbreed, patients should drink plenty of water, ground urination, often to flush the bladder and urethra.
Purpura nephritis, dietary requirements, the requirements of the salt
Henoch-Schonlein purpura nephritis patients without edema or hypertension do not haveto salt restriction. Limit salt intake in patients with edema and hypertension, not limited tosalt may aggravate sodium retention and edema are hard to dismiss, causing high blood pressure. General every day, control salt 2-3 grams, oliguria, elevated serum potassiumshould limit the potassium salt intake.
Purpura nephritis, dietary requirements, taboo food
Allergy foods, fried foods, aquatic products such as shrimp, crab, spicy foods such aschili, garlic, raw onions, parsley, dog, horse, donkey. Mainly in low-salt diet, light foods rich in vitamins, different types of patients may be appropriate to add a little seasoning,such as a small amount of sesame oil, MSG and other.

IgA nephropathy is why permanently?

IgA nephropathy will be permanently Why? Why doctors symptomatic drugs prescribed by that time well now committed? Study the root causes, treatment can only see the appearance, not simply start taking medication, no hematuria, in fact, general doctor of medicine western medicine tired hormone substances, Western medicine is only symptomatic treatment, that Western medicine is just to eliminate the hematuria did not repair the damaged kidney, so the drug is stopped here there would hematuria.
Hematuria, the real reasons of IgA nephropathy: kidney consists of five intrinsic cells generated with IgA nephropathy is mesangial cells inherent in the kidney cells proliferation, it is also called the iga type mesangial cell hyperplasia.
Then, the blood in the urine of IgA nephropathy is how to generate? Susceptible populations of IgA nephropathy is defective mucosal immune function, when mucosal decreased immune function, very prone to upper respiratory tract infection or gastrointestinal infection, those antigens (inflammatory substances such as bacteria, viruses) enter the body and the body iga inflammatory response constitute the IgA immune complexes, leading to large amounts of immune complex deposition in glomerular mesangial cells District as pathogenic factors invade makes mesangial cell proliferation proliferation, inflammatory substances continue to stimulate mesangial cell dysfunction, and mesangial cell function is swallowed, the physiological function of macromolecules decreased, making the red blood cells leak more and more, and ultimately is occult blood in a single laboratory has been increasing.
IgA nephropathy hematuria how to treat? Of IgA nephropathy why permanently? Purely traditional treatment In order to eliminate blood in the urine, as in a short period of time will inhibit the development of the disease, however, the real onset of the reasons has not been eliminated, good scar is also pain, how to cure blood in the urine?
The emergence of blood in the urine of IgA nephropathy nephropathy due to invasion of external inflammatory substances cause damage, so in the course of treatment will be carried out anti-inflammatory, inhibiting inflammatory substances continue to be intrinsic cells of the kidney mesangial cell damage; external inflammatory substances into the human body with IgA antigen-antibody immune complexes, and then deposited in the glomerular mesangial area, kidney ischemia and hypoxia, and thus do the vasodilators to improve blood circulation and kidney ischemia hypoxic state to provide a good treatment for the repair of mesangial cells; inflammatory cells that would increase blood viscosity increased, the platelet hyperfunction, enhanced coagulation, resulting in the micro thrombosis composition, in order to prevent microthrombi composition, and thus to anticoagulant therapy, maintaining smooth blood to avoid the excessive deposition of immune complexes; inflammatory cells of IgA immune complex deposition led to an increase in mesangial cell proliferation, atrophy, and cell extracellular matrix, and therefore must extracellular matrix deposition degradation, so that it can be excreted with the urine. The above inter-related treatment, IgA nephropathy hematuria before it can be restored to normal.
IgA nephropathy why permanently? Overall the treatment of IgA nephropathy hematuria can not simply eliminate the hematuria, and should thus be treated, to repair damaged kidney mesangial cells, as will be made in the treatment of a multiplier effect, the other IgA due to immune dysfunction, kidney patients need time to prevent some of the invasion of bacteria, viruses, that is, to prevent colds and infections, I believe, IgA nephropathy will soon be recovered by treatment of science and daily life cautious.

The FSGS type iga nephropathy How effective treatment?

The FSGS type iga nephropathy How effective treatment?
IgA nephropathy is now ring out acyl flushing and hormonal therapy, was discharged due to the protein drop does not go home medication two days ago went to read Chinesenow drink and herbs can be? Eat hormone methylprednisolone and antihypertensive drugs Diovan and enalapril? How is it treated?
"How effective type of FSGS iga nephropathy treated?" Response
You are suffering from iga nephropathy FSGS is focal stage of hardening, long-term oralmedicine side effects of the body can not be ignored, and traditional Chinese medicineoral onset is slower. The above mentioned drugs are immunosuppressants, usually can control the symptoms and indicators, side effects are more suitable for long-term use fortreatment of now the key is to repair the damage of the control of symptoms at the sametime repair the kidney pathology protein and red blood cells and thus prevent leakage.So that the protein continued to leak not only can cause hypoproteinemia, severe also affect renal function, it is best to nephropathy specialty hospitals, the standard treatment,this will be more targeted. The key to the treatment from the treatment of kidney start to reach good results. Infiltration therapy of micro-based traditional Chinese medicine can be considered depending on your situation, not only remove the immune complexdeposition in the glomerular filtration membrane and diseased tissue, but also to repairglomerular filtration membrane and improve its permeability through the repair proteinand occult blood disappear naturally, not easy to relapse. As for which treatment optionsbut also your own according to their own situation specific choice, as long to find the most appropriate for your illness, treatment options, together with your usual diet control and regular exercise, you a big step toward rehabilitation.

FSGS can cure you? How to treatment

Patients:
Gender: Male Age: 17
Occult blood 2, there are a lot of my protein proteinuria, FSGS can be cured right? How to treatment?
Doctor:
Past, that the poor efficacy of the disease, treatment is difficult, there is no mature andeffective treatment, patients are generally 5 to 10 years into the renal failure of treatmentare still disputing of FSGS. In recent years, a large retrospective study showed that theremoval and treatment of the cause of FSGS etiology, diuretic, antihypertensive,symptomatic treatment can promote the remission of nephrotic syndrome, and preventand delay the progression of the disease. The clinical observations to extend theremission rate of hormone treatment increase of FSGS.
The advice may be the treatment of Integrative Medicine recommended that the mainlight diet, eat high-protein high-fat, high salt foods forbidden to eat spicy spicy food in the diet; exchange in their daily lives in the season when attention to the timely change of clothing, in order to avoid the cold caused the aggravation or recurrence of disease,attention to such as rest and more rest.

Greek patient with kidney disease in China

FSGS treatment

What is of FSGS? Stands for focal segmental glomerulosclerosis, an onset of nephrotic syndrome in children and adolescents, but also result in adult renal failure.
How to the treatment of FSGS? Why not promote the use of hormones? Proteinuria, a small ball hardening process of renal fibrosis due to FSGS appear, treatment, clinical medication Western conventional hormone immunosuppressive agents, such as hormones prednisone, to plug The betamethasone A strong nylon, etc.; commonly used immunosuppressants such as cyclophosphamide, tripterygium. These drugs can play an anti-inflammatory effects, but to control the disease is not only anti-inflammatory, but also expansion of the renal artery at all levels to solve the problem of renal hypoxia, but also anticoagulant, dilation of blood vessels after blood flow, but also degradation of glomerular sclerosis, to solve the problem of the filtration membrane, the above problem solving, as well as to impaired filtration membrane repair, only repair place, like proteinuria such external manifestations in order to completely disappear. For the treatment of FSGS, the hormone treatment not only side effects, the effect is often not ideal. So should resolve the issue will be a comprehensive treatment measures.
At the same time, the living diet should have a scientific system to develop programs to cope with the treatment of major principle with other nephropathy is a light diet, low salt, low fat, a small amount of high quality protein to avoid hot and spicy, the details mustbased on individual circumstances to the specific formulation.
The effect of micro-medicine treatment of FSGS? Micro-based medicine treatment and traditional treatment methods differ from traditional treatment methods tend to be directly aimed at the elimination of proteinuria to start, we are not at our hospital to treat the root cause for the cause of proteinuria. That is the focus of the treatment on the repair of the epithelial cells and mesangial cells.
Treatment measures is the integrated use of vasodilators, anti-inflammatory, anticoagulant, and measures of degradation of harmful substances. On the use of drugs, we are not simply use the single treatment of Chinese and Western medicines, but to maintain the foundation of Western medicine treatment to increase efforts to TCM treatment, and a new combination of methods, in addition to our treatment a major feature of our hospital in order to improve the efficacy of traditional Chinese medicines and the development of the hospital preparation, and that these agents played an important coordinating role in the process of TCM and Western medicine treatment. That treatment effects are very different.
We call this method: micro-based medicine blocking renal fibrosis infiltration method.Practice has proved that this treatment we can determine the exact effect of the repair of the glomerular capillary epithelial cells: damage to epithelial cells can be repaired, the condition will get better, "disease" is getting better, epithelial cell function will be restored, restore the function, proteinuria will naturally disappear. This function after the resumption of proteinuria disappeared, then the probability of recurrence will reduce.

Note: in the daily life of patients with kidney disease

1.A fresh light digestible food, avoid seafood, beef, lamb, spicy food, wine and all the fat things such as: spiced aniseed, coffee, coriander.
2.Prevent colds, to avoid the cold, not tired, do not eat health food, tonic, to prevent angryheavier.
3.Edema, weight should avoid salt, limit the intake of protein food, less water. Edema isnot heavy into the low-sodium drink; swelling does not limit the intake of water andprotein foods.
4.Microscopic hematuria easily lit by the water, eat more apples, sugar, black sesame seeds, fungus and other nourishing yin and down as food.
5 hyperkalemia were cut high-priced foods such as seafood, mushrooms, ham,mushrooms, dried fruit, corn flakes, banana, citrus, potatoes, dried radish, tea, soy sauce, monosodium glutamate and other.
6. High blood uric acid, especially not eat animal offal, Xiaxie mussels, beer,mushrooms, beans, spinach.
7 patients with chronic nephritis can drink milk, 1 egg, 2 lean meat.
8.Hypertension should serve antihypertensive drugs to control blood pressure, those taking hormones, under the guidance of the physician in descending amount of acidosis shouldbe taking sodium bicarbonate to correct acidosis.
9.Disable, neomycin, streptomycin, gentamicin, Guan Mu Tong, fangchi, aristolochic andauto-immune injection.
10 confidence, and adherence to treatment, to keep the peace of mind, optimism.
11 married patients with sexual restraint.

Children with nephrotic syndrome diagnostic criteria

The nephrotic syndrome is due to increased permeability of the glomerular filtration membrane, leading to a clinical syndrome caused by a large number of plasma albumin is lost in the urine. ?? Has massive proteinuria (qualitative> + + + 24hr quantitative> 50mg/kg); hypoproteinemia (plasma albumin <30g / L); ƒ hypercholesterolemia (blood cholesterol> 5.72mmol / L), ; "varying degrees of edema, four major characteristics. Beijing Military General Hospital, subsidiary Bayi Children's Hospital, Pediatric Nephrology, Huang Jianping variety of primary, secondary, congenital or hereditary glomerular diseases can cause this disease, but children period the vast majority (90%) of the primary.
1 clinical classification
(1) simple type only these four characteristics.
Nephritis (2) In addition to the above conditions, but also with one or more of the following four:?? Hematuria: 2 weeks three times centrifuged urine check, red blood cells> 10 / HPF; recurrent or persistent hypertension, 317.3/12.0kPa school-aged children, preschool> 16.0/10.7kPa, and the exclusion of corticosteroids due; ƒ persistent azotemia, blood urea nitrogen 10.7mmol / L, and the exclusion of hypovolemia due topersons; the total blood complement or C3 repeatedly reduced.
2 pathological type
Common pathological type of minimal change disease (MCD) and non-minimal change disease, the latter including focal segmental glomerulosclerosis (of FSGS), mesangial proliferative glomerulonephritis (MsPGN), membranous nephropathy (MGN) and membrane proliferation of nephritis (MPGN). The children MCD common, followed by FSGS and mild to moderate MsPGN. MGN is rare in the pediatric primary, only 1 to 2 percent, the vast majority of the secondary, especially hepatitis B virus associated glomerulonephritis. MPGN is a more serious type of pathology, and need early diagnosis and treatment in a timely manner.

Brief for FSGS

FSGS refers to the glomerular capillary loops focal segmental sclerosis or hyaline degeneration, no significant cell proliferation of the glomerular capillary. May as the Department of
Mesangial proliferation, mesangial IgM deposition, and focal glomerulosclerosis, but minimal change nephropathy resistant to steroids, the consequences of recurrent chronic progress. There are also hormone invalid primary nephrotic syndrome of early renal biopsy is the focal glomerular sclerosis. Therefore, whether the disease as an independent glomerular disease is still controversial. However, representatives of other kidney disease type of clinical pathology, or as an independent disease, more common, and there is a growing trend.
(A) the primary focal glomerulosclerosis of unknown etiology.
(B) secondary focal glomerulosclerosis
1, glomerular diseases, heroin-associated nephropathy, tumor-associated nephropathy, diabetes, AIDS, hereditary nephritis, IgA nephropathy, preeclampsia and Hodgkin's disease.
2, tubular, interstitial and vascular disease, reflux nephropathy, radiation nephritis, analgesic nephropathy, and sickle cell disease.
3, other renal hypoplasia, obesity and old age and so on.
Not yet clear. Majority view that glomerular hemodynamic changes or basement membrane damage causes the ball mesangial overload intake the macromolecules caused by glomerular sclerosis. Human embryonic near medullary nephron occur early, large size, high filtration rate, capillary high-pressure, high filtration eventually lead to structural damage, the disease nearly medullary nephron damage early and severe.Segmental glomerular epithelial cell damage, the basement membrane anionic electrical barrier damage, chronic proteinuria overload, sustained high filtration, high perfusion will eventually lead to glomerulosclerosis. Glomerular hypertrophy and foam cell generation is important in the formation and development of the disease. 5/6 nephrectomy animal model, the glomerular capillary plasma flow and pressure, glomerular epithelial cells was significantly impaired in residual nephron hyperthyroidism, leading to hyalinization. Fogo primary focal glomerulosclerosis pathophysiology and clinical phase, it was found that the average glomerular area of ​​adult and children patients was significantly greater than the minimal change of the same age. Repeat renal biopsy also confirmed that some of the disease, expressed initially as small lesions, glomerular hyperplasia. Be seen in many patients with primary focal glomerulosclerosis, glomerular foam cells, it has the characteristics of the macrophage group, can be transformed by circulating monocytes or mesangial cells. Some cytokines and growth factors such as IL-1 alpha-TNF, IL-6 may play a role in the lead to glomerulosclerosis. There are animal studies found that serum cholesterol levels are related with the degree of hardening.
Immune damage is also involved in the occurrence and development of the disease, the immune pathological the glomerulosclerosis area visible IgM and C3 granular deposits. Electron microscopy showed sclerosis lesions have a large number of electron dense deposits. And the disease to recur in kidney transplantation.
(A) general treatment performance for massive proteinuria, edema, given the low-salt diet, the proper use of diuretics. Hypoalbuminemia obvious, appropriate use of albumin.High blood pressure significantly, sodium restriction, diuretic invalid, can be added, such as angiotensin converting enzyme inhibitors, calcium antagonists and other antihypertensive drugs.
(B) of hormones and other immunosuppressants
1, the hormone to nephrotic syndrome as the main performers, especially the original biopsy for small lesions, the development of focal segmental glomerular sclerosis, is still the preferred hormone, mostly favorable response, adult dosage, prednisone 0. 5 ~ 1mg / (kg · d), 6 to 8 weeks, then gradually reducing over to every other day therapy, the total course in one year or more. Pei reports prednisone for treatment of primary focal glomerular sclerosis, the complete remission rate of up to 47% of these patients 5-year kidney health survival rates significantly higher than the responders (96% vs 55%).Although there the data hormone plus cytotoxic effect is not better than a single hormone.However, most scholars advocate invalid, on the hormone-dependent and recurrent episodes should combination therapy. Cytotoxic drugs can significantly reduce the relapse rate and extend remission. And reduce the amount of hormones, and reduce its side effects. More choice of cyclophosphamide intermittent intravenous injection, total dose of <150mg/kg. Also oral chlorambucil In recent years, also with cyclosporine A treatment of this disease, recently some efficacy in the reduction or withdrawal process to recur. Expensive and potentially nephrotoxic, it is not appropriate for the drug of choice.
(C) treatment of angiotensin-converting enzyme inhibitor not only lower blood pressure, and can reduce urinary protein may be beneficial to delay renal failure. In addition, the disease associated with nephrotic syndrome is not only high-clotting disorder, there intrarenal coagulation, balloon adhesion, should be the anticoagulant therapy, such as: dipyridamole 25 to 75mg / d, China Flynn 2,5 mg / d can reduce protein urine, improve renal function.

FSGS's treatment progress

Advances in the treatment of nephrotic syndrome, focal segmental glomerulosclerosis FSGS is one of the main reasons of the adult nephrotic syndrome, accounting for 15 to 20 percent of the adult nephrotic syndrome. FSGS is not an independent disease, but has many causes and pathogenic mechanisms and the type of tissue injury, a clinical and pathological syndrome. In 1957, Rich first FSGS pathology description, until the 1970s FSGS only as a clinical and pathological syndrome is listed. FSGS as one of the most common type of renal biopsy pathology, pathological type, further refinement is divided into five sub-categories. The differential diagnosis of primary and secondary FSGS, contribute to the treatment of FSGS. Past that FSGS hormone resistance, but recently with the improvement of the treatment, this situation has been improved. This article discusses the etiology, diagnosis, treatment and prognosis aspects of FSGS.
FSGS in the pathophysiology of FSGS is a descriptive diagnosis, not a disease of independence. Primary of FSGS, I do not know the cause of the secondary of FSGS (underlying cause) and pathogenesis are not fully understood, gradually profound secondary FSGS research, understanding the mechanism of primary FSGS. That the loss of secondary FSGS and renal units, high filtration and glomerular pressure and other cause renal decompensation response. Nephrectomized animal experiments to prove that the loss of podocytes is a key factor in FSGS renal decompensation response, and animal experiments confirmed the the FSGS existence of glomerular high perfusion, increased pressure within the phenomenon of hypertrophy or glomerular. That the secondary FSGS pathogenesis are as follows: Start the factors that damage podocytes, damaged podocyte detachment from the basement membrane and enter the capsule, because of foot cells can not regenerate, so that the basement membrane exposed capsule of the parietal epithelial cell adhesion on the bare basement membrane capillary climb and Bowman's capsule adhesion, and ultimately the formation of adhesion of the parts of the parietal epithelial cells and capillary climb the formation of cavities, if the adhesion of the capillary is still functional, the filtered fluid leakage into the cavities, these filtration the liquid leakage of the capillary, as fiber cells by filtrate stimulation, eventually leading to glomerular matrix fibrosis. If this leakage and loss of podocytes continued to exist, and finally to renal interstitial fibrosis, capillary collapse, adhesion, hyalinization and micro-thrombus gradually increased. According to the cause of secondary FSGS is divided into: 1). Family: ɑ-Actinin 4 defects; of nephrin defects; podocin in defects; WT-1 defects; carrying CD2AP and its defects, mitochondrial disease. 2) virus: HIV-related kidney disease, parvovirus B19 infection. 3) drugs: heroin nephropathy; interferon-ɑ; lithium; ammonia hydroxyl disodium phosphate, or alendronate. 4) high perfusion or hypertrophy lead to adaptive changes: congenital kidney to reduce single disease with compensatory hypertrophy; unilateral renal agenesis; renal cortical necrosis; reflux kidney disease; kidneys after surgical resection; chronic allograft nephropathy ; 5) non-specific scarring of the glomerular disease: focal proliferative glomerulonephritis, hereditary nephritis, membranous nephropathy, thrombotic microangiopathy. 6) lymphoma. 7) Other: diabetic nephropathy; hypertensive nephropathy; obesity; congenital cyanotic heart disease; anemia. The pathophysiology of primary FSGS is not clear, but there is evidence that circulating factors in the blood change the glomerular permeability [5].Previous studies have shown that the disease will relapse FSGS patients after renal transplantation, a few days after transplantation of patients in proteinuria can occur after plasma exchange can lead to proteinuria mitigation [6]. Literature that the increase in glomerular permeability may inhibit the permeability factor is missing or lost related.Animal and human studies results suggest that primary FSGS pathogenesis may be as follows: podocyte injury induced foot process effacement, proteinuria, and microvilli transformation, without loss or loss of podocytes, parietal epithelial cell injury, proliferation, and surrounded by the renal The ball capillary loop, and parietal epithelial cells secrete extracellular matrix lead to scar formation. However, the mechanism leading to the proliferation of parietal epithelial cells is unknown, the final activation or injury in podocytes and parietal epithelial cell activation or injury of the interaction lead to FSGS formation.
Primary and secondary FSGS differential diagnosis of primary and secondary FSGS differential diagnosis contribute to their treatment options. In general, medical history, laboratory tests may provide clues in order to facilitate the differential diagnosis. The kidney comprehensive level of proteinuria, plasma protein is an important indicator to identify the primary and secondary FSGS. [10] prompted the plasma protein <30g / L, more inclined to the primary of FSGS,> 35g / L were more inclined to obesity, reflux nephropathy, or kidney was removed secondary of FSGS. Should be noted that, in the case of secondary FSGS virus-associated FSGS, drug-related FSGS and familial FSGS, plasma protein <30g / L,. A recent study [11] showed that primary and secondary FSGS patients with foot process fusion extent inconsistent, primary FSGS foot processes to the degree of integration than the secondary FSGS weight, and foot process width compared with secondary FSGS wide foot process width and type of FSGS is not dependent on the degree of proteinuria. For patients with familial FSGS, the podocyte-related protein gene can be detected defects, adult podocyte protein gene defects than children, its defects-positive rate of about 1.5 to 5.0%, available for detection of gene ɑ-Actinin of nephrin, podocin in WT-1 and CD2AP, the current study more ɑ-actinin4 and the podocin gene defects [12,13].
China Medical Nephrology credits 2010 Annual Conference seminar is a compilation of the thematic reports lead to the diversity of its clinical features and natural history of inconsistent diagnostic criteria of the previous FSGS. Secondary to hyperperfusion FSGS less renal biopsy, clinical research is less likely to be mentioned. This article focuses on the clinical and prognosis of primary FSGS. FSGS can occur at any age, but adults mainly aged 40 to 50-year-old, male to female ratio of 1:1. Primary FSGS, secondary to infection, drugs or genetic defects in FSGS manifests itself in nephrotic syndrome; hyperfiltration secondary FSGS clinical manifestations often relatively hidden, and even urine protein of more than 3 to 4g / d, but no significant hypoproteinemia or edema [14]. In addition to proteinuria, microscopic hematuria and hypertension, whether primary or secondary FSGS are very common.
On the other hand, a recent randomized controlled trials to prove that cyclosporine effectively. 75% with only 22% of the placebo patients into remission by disease mitigation. A year later, the cyclosporine group, 48% remained in remission and the placebo group, only 13% of the disease is still in remission. It is noteworthy that no patients discontinued because of adverse side effects. Similarly, randomized controlled trials also found that the abnormal renal function or worsening, membranous nephropathy, patients can still benefit, proteinuria will decline, deterioration of delay; with cyclosporine A year later, the efficacy of half of the patients able to maintain at least two years . However, cyclosporine is still inadequate: expensive and can cause kidney damage.
Experts: wet, hot (cold), drugs, and silt blocking the function of organs wasting leads to kidney cloud cult poison the block to proteinuria, occult blood, serum creatinine, blood urea nitrogen increased as the main performance, wasting Spleen kidney damage based. Spleen renal damage, proteinuria, occult blood, serum creatinine, blood urea nitrogen standard. Evil gather scattered the main aspects of conflict, Xie Sheng leading direct cause of renal failure aggravated, banishment of evil spirits for the basic treatment principle, from the immunological point of view is to promote retention in glomerular immune complexes while the discharge, and enhance the kidney function of a lid, to reach the repair of natural toxins (creatinine, blood urea nitrogen), urine protein, occult blood, tube gradually disappear. Between them there are complementary and interdependent dialectical relationship. Therefore, lowering cloud detoxification, Jianpiyishenfang, the principle of the entire course of treatment. Jiangzhuo restore therapy departure from the etiology and pathogenesis of kidney disease, uremia, the use of specimens to take into account the dialectical differentiation of ideas to improve a single therapy session of the Chinese medicine blood stasis, tonifying. Corrected dialysis Western session palliatives. Fang Akebia, rhubarb, Pinellia the Chinese medicine clinical practice prejudicial to the blood of the drug does not do prescription dialectical side certificate corresponding rule is compared with chronic renal failure and kidney yang, and advocated Onyang ; compared to the Western term dialysis therapy, are a large step forward.

Do not want to reuse hormone, how to treat?

For the treatment of FSGS kidney disease, current clinical is still a lack of effective measures. Western medicine clinical application of hormone combination therapies for treatment. Corticosteroid therapy, a small number of patients with FSGS kidney disease (30% - 40%) of the condition can be eased. However, long-term use of hormone, there will be a lot of side effects attendant. Indeed, a large number of side effects of hormone produced by kidney patients on the treatment of their disease has concerns about the mental. Especially after the application of hormones or immunosuppressive agents in kidney patients discontinued the course of medication in the face of the predisposing factors (such as colds, fever, fatigue, allergies, etc.), kidney disease condition is very easy to relapse and increase.
Typically, FSGS kidney patients face hormone inevitably there are concerns about the psychological. Therefore, in search of better treatment methods, to avoid the side effects of hormones, become the common aspiration of the FSGS kidney patients. In fact, the micro therapy for the penetration of traditional Chinese medicine to break this traditional treatment model. Why do you say? Infiltration therapy of micro-based traditional Chinese medicine can effectively block the fibrosis of the kidney lesions, activation of cells in lesions of the kidney metabolic function, and mentioned the necessary nutrients as well as the rebuilt repair and reconstruction of damaged kidneys. Kidney area skin penetration into the body of the micro-penetration therapy of Chinese medicine to improve the repair environment can damage the kidneys, the gradual recovery of kidney disease, glomerular effective filtration, enhanced compensatory ability of the kidneys of healthy cells. In this way, the root causes of nephropathy proceed slowly to restore renal function, fundamentally eliminate the patient's urine protein.
However, for Miss Jiang is now applied hormone therapy, hormone medication principle limit, not the temerity to disable the hormone drugs. Because the hormone withdrawal there is a pattern, sudden withdrawal can cause hormone arrest reaction, exacerbate kidney disease. Therefore, you want to really get rid of the hormone, wants to fundamentally cure kidney disease, should be gradual infiltration therapy in the application of micro-based traditional Chinese medicine treatment of kidney disease during hormone dosage reduction, and ultimately achieve the purpose of treating kidney disease and completely get rid of the hormone.

What is the FSGS kidney disease? What are clinical manifestations of FSGS kidney disease?

Glomerular capillary nephrotic FSGS kidney disease called focal segmental glomerulosclerosis whole, refers to the glomerular capillary loops with focal segmental glomerular sclerosis or hyaline degeneration, no significant cell proliferation. FSGS kidney disease is a common pathological type of primary nephrotic syndrome, the pathological type 50% of patients with nephrotic syndrome FSGS kidney disease, renal biopsy can be clear of the disease.
The disease mostly occurs in children and young people, more men than women, a small number of patients with FSGS kidney disease before the onset of upper respiratory tract infection or allergic reaction history. In addition, the occurrence of FSGS nephrotic familial tendency FSGS kidney disease is relatively common in the atopic population, the main clinical manifestations and characteristics:
(1) The first clinical symptoms of nephrotic syndrome, microscopic to common hematuria, and occasionally gross hematuria in adults is about 2/3 of patients had mild persistent hypertension.
(2) urine routine examination, a small number of patients with FSGS kidney disease is asymptomatic proteinuria. Proteinuria and the vast majority of non-selective, but early high or moderate selectivity.
(3) blood test serum C3 levels were normal, IgG levels decline.
(4) of FSGS kidney patients more than the performance of the proximal renal tubular dysfunction, progressive decline of glomerular filtration rate, upper respiratory tract infection or allergic allows a variety of symptoms get worse.

Focal segmental glomerulosclerosis should do what?

A urine routine examination, microscopic hematuria, proteinuria, and often aseptic white blood cells in urine, grape diabetes. Impaired renal tubular function, urinary amino acids and phosphate in urine, its high incidence of other types of NS.
Blood tests have significantly lower serum albumin, serum albumin is usually less than 25g / L, and a few up to 10g / L below. Decline in glomerular filtration rate (GFR). BUN, creatinine increase. The majority of patients with hyperlipidemia. Serum C3 is usually normal IgG level decreased, C1q is mostly normal. 10% ~ 30% of patients positive for circulating immune complexes. Hypovolemia can cause the increase in hematocrit.Normal white blood cells and classification. Platelets slightly elevated. Water retention will result in lower sodium concentration, the long period of sodium or acquired adrenal insufficiency, can lead to lower sodium concentration. Hyperlipidemia can cause pseudo-hyponatremia, and platelets in vitro release of potassium ions, thrombocytosis can also cause pseudo hyperkalemia.
A renal biopsy light microscopy typical FSGS lesions characteristic focal segmental glomerular damage, lesions involving a small number of glomeruli and glomerular some segments of hyaline sclerosis. The lesions are often deep from the cortex or nearly medullary parts of the glomerulus began, and gradually extended to the renal cortex.Glomerular lesions showed segmental glomerular sclerosis, uninvolved normal of glomerular mesangial matrix increase. Hyaline material deposited in the damaged capillary loop endothelial cells, hardened area with occasional foam cell formation, proliferation of epithelial cells of the common limitations. Early lesions may only local epithelial cells and basement membrane from the epithelial cell swelling, vacuolar degeneration, basophilic cytoplasm. Hardening of the capillary loop wall adhesions with Bowman. Each segmental glomerular damage of a different range of disease progression may contribute to global sclerosis. Fully developed cases of lesions, easily mistaken for the "non-specific chronic sclerosing glomerulonephritis, and through immunofluorescence differential diagnosis. Renal tubular damage often appears as a focal thickening of the basement membrane and atrophy. Coexist, such as focal tubular damage and mild glomerular changes should be suspected of FSGS. Renal tissues of focal, global glomerulosclerosis FSGS often late performance, associated with severe tubulointerstitial lesions in pediatric patients up to 30%. The typical adult hormone-sensitive minimal change can be seen a small number of global sclerosis of glomeruli, with FSGS phase difference. In addition to primary FSGS, many diseases of the kidney tissue can be seen the similar FSGS change. FSGS may also overlap with primary glomerular diseases.
Electron microscopy a large number of proteinuria cases most or all of the glomerulus shows diffuse or segmental foot process change. Early visible in the capillary wall and (or) mesangial foam cells, mesangial matrix increase and part of the capillary collapse.Endothelial cells and mesangial area corresponding to the electron dense deposits, mesangial cell proliferation, large electron-dense material under the light microscope hyalinization and immunofluorescence IgM and C3 deposition. Ball collateral membrane area and endothelial cells can also be found fine granular electron dense deposits.
3 immunofluorescence sclerosis or necrosis can be found in the C3 or IgM and C1q was irregular, granular or nodular distribution. Glomerular lesions were negative. Occasionally mesangial have IgM and C3 distribution and IgG, IgA, rare.

What are the early symptoms of focal segmental glomerulosclerosis?

The disease mostly occurs in children and adolescents, men slightly more than women. A small number of patients before the onset of upper respiratory tract infection or allergic reactions. Most common clinical symptom is the nephrotic syndrome, about 2/3 of patients with massive proteinuria and severe edema, urine protein 1 to 30g / d, more than about 50% of patients with hematuria, microscopic hematuria common and occasionally gross hematuria. 30% to 50% of the adult patients with mild persistent hypertension or manifestations of chronic nephritic syndrome, patients with 24h urinary protein <3.5g / d, obvious edema, often hematuria, hypertension and renal insufficiency, while more than 50% were kidney ensemble performance significantly "three high and one low clinical manifestations. A small number of patients with no obvious symptoms, and occasionally found in routine urinalysis proteinuria. This type of asymptomatic proteinuria sustainable a long time, a better prognosis. A small number of patients with this type of gradual development of end-stage renal failure. Proteinuria and the vast majority of non-selective, but early high or moderate selectivity. Serum C3 levels were normal, and IgG levels decline. Often proximal tubular function is impaired performance.The above symptoms of upper respiratory tract infections or allergies can make worse.
Slight differences in the different pathological types of clinical manifestations of the disease, typical FSGS and glomerular hypertrophy, urinary protein less; cell FSGS often massive proteinuria (> 10g / d), and prone to renal insufficiency. Reported that 60% of the cells in FSGS patients with serum creatinine> 2mg/dl, while only 10% of patients in a typical FSGS serum creatinine increased. Collapsing type of FSGS also significant proteinuria, often> 10g / d and renal insufficiency are more serious than other types, and hypertension is relatively small. This type of rapid onset, rapid progression, usually 1 to 2 years after the onset into the end-stage renal failure (ESRF).
The clinical manifestations of pediatric patients and adults, mostly with nephrotic syndrome, while the proportion of the occurrence of hypertension and renal insufficiency than in adults is low. The majority (40% ~ 60%) of FSGS was chronic progressive progress, eventually leading to kidney failure, a small number of patients (10% to 15%) rapid progress of the disease, earlier onset of renal failure.
The diagnosis clinically and there is no reliable indicators should rely on renal biopsy in the diagnosis of FSGS and pay attention to rule out all possible secondary factors, such as HIV infection and drug abuse. Asked in detail about the history, physical examination and laboratory tests are helpful in differential diagnosis. For example, the performance associated with proximal renal tubular dysfunction in patients with nephrotic syndrome, or simple proteinuria; persistent nephrotic syndrome with hypertension, microscopic hematuria, non-selective proteinuria; hormone-sensitive patients should be suspected of FSGS. Renal biopsy examination can help diagnose typical focal segmental glomerulosclerosis (FSGS) characteristics for focal damage, the local impact of a small number of glomerular (focal) and glomerular (segmental). Start at nearly the medulla of the glomerular involvement, mild cases involving only a few capillary loop, re-spread to most of the glomerular lesions were uniform without cells or minimal hyalinization substance (within the loop foam cells, transparent drops), and severe cases, the balloon adhesions, visceral epithelial cell proliferation to form a "cap-like" structure, or even the "umbilical" lesions. Another focal glomerulosclerosis. The involvement of tubular epithelial cells of the nephron often shrinking, the surrounding matrix, see cell infiltration, fibrosis. Electron microscope, most of the glomerular or glomerular foot process effacement, epithelial cells and their foot processes and basement membrane from the endothelial cells and mesangial electron dense deposits at. Immunofluorescence in the hardened area to see IgM and C3 were irregular lumps, nodular deposition. Glomerular lesions were negative or diffuse IgM, C3 deposition, IgA, IgG rare. The disease often misdiagnosed as minimal change nephropathy, and it requires a combination of clinical manifestations and renal histological findings and response to hormone therapy and presence of spontaneous remission or drug induced remission in fully taken into account.Help the differential diagnosis of FSGS and MCD. Glomerular focal segmental sclerosis seen in FSGS can also be found in the development of a variety of chronic kidney disease, such as obstructive nephropathy, reflux nephropathy, AIDS patients and diamorphine addicts; can even be found in obese persons. Therefore, a comprehensive analysis to make the right diagnosis.

Focal segmental glomerulosclerosis is caused by what?

(A) causes
The FSGS There are many risk factors. Injury such as poisoning, humoral and hemodynamic changes can lead to the damage of the capillary wall, so that the macromolecular protein and retention, and immunoglobulin deposition and then combined with C1q and C3, causing the degeneration of the podocytes and the basemembrane detachment. The study found that the phenotype of podocytes in primary FSGS has changed. Damage of the epithelial cells is unclear capillary loop collapse and sclerosis of FSGS may be a manifestation of epithelial cell lesions increased tissue repair. Focal sclerosis lesions rapid recurrence after renal transplantation, indicating that systemic factors in the pathogenesis of FSGS.
Residual nephron hemodynamic changes, cause the compensatory glomerular capillary hypertension, hyperperfusion and hyperfiltration, resulting in damage epithelial cells and endothelial cells, mesangial cell dysfunction, leading to progressive focal sectionsegmental sclerosis. This pathological process is aggravated by ingestion of a large number of proteins, limit protein intake and blood pressure lowering treatment and reduce the Endothelial cell damage caused by platelet aggregation and microthrombosis, and increase the development of lesions; occurrence and the pathogenesis of many of FSGS, such as chronic streptococcal infection, glomerulonephritis, chronic renal allograft rejection, reflux nephropathy and analgesic nephropathy. In addition, it is also observed near marrow glomerular glomerular filtration rate than the cortex glomerulus, but also support the hemodynamic changes of FSGS risk factors.
Drug abuse and AIDS can cause typical FSGS nephrotic syndrome and progressive renal failure, it can be the final outcome of most of the proliferative glomerulonephritis.However, the majority of cases are idiopathic, pathological type was of FSGS is found when the first renal biopsy.
Segmental glomerular sclerosis in addition to be found in FSGS, also can be the final result of the proliferative glomerulonephritis (eg, glomerulonephritis) or related with hyperfiltration in nephrotic syndrome, some patients go through a Bureau stove segmental proliferative phase, the formation of segmental necrosis and scarring, this situation is common in secondary glomerulonephritis.
(B) in the pathogenesis
The pathogenesis of this disease is inconclusive, only a series of observations and inferences:
A mesangial uptake of macromolecules excessive study found that to test the animal intravenous injection of exogenous protein, can cause changes similar to the disease, suggesting that long-term heavy proteinuria can lead to damage of the epithelial cells, glomerular mesangial cells over- load to the development of glomerular focal segmental sclerosis.
Glomerular hemodynamic changes in glomerular capillary loop Benbingfasheng in high-pressure role is very important. Studies have shown: the animal model of part or most of nephrectomy, the remaining renal tissue of six months or so that the focal segmental sclerosis. Prompted the disease to occur may be related to hemodynamic changes. The mechanism may be compensatory capillary hypertension in the remaining kidney tissue, as well as the goals, the expansion of the efferent arteriole, glomerular capillary loop completely open to the systemic circulation, resulting in glomerular hyperperfusion, high transmembrane pressure, filtration The increase in protein and other soluble molecules, causing capillary loop epithelial and endothelial cell injury and mesangial cell dysfunction.Given, such as diet control or angiotensin-converting enzyme inhibitor therapy, so that high pressure in the glomerular capillary to reduce the development of focal segmental sclerosis moderated, this is better able to explain the glomerular capillary loop HV role.
3 hyperlipidemia disease, development, and hyperlipidemia was positively correlated.The study found: (1) increase in food fat can test animals glomerular sclerosis, glomerular lesions and elevated blood lipids to the same extent. ② congenital growth process of obese rats natural occurrence of focal segmental glomerulosclerosis. ③ to lipid-lowering drug therapy, with the decline in blood lipids, glomerular damage also reduced. (4) human obesity associated with blood cholesterol, triglycerides increased and cardiac hypertrophy, and kidney, there may be similar to the primary focal segmental glomerulosclerosis lesions. Such cases, the control diet, weight loss weight loss, followed by reducing urinary protein nephrotic syndrome can be eased.
Hyperlipidemia cause glomerular focal segmental sclerosis may be mesangial cells have the ability to intake of low-density lipoprotein (LDL), oxidized LDL receptor on mesangial cells, and therefore glomerular uptake of oxidized LDL and oxidized LDL is a lipoprotein lead to hardening of the arteries of the most toxic. LDL stimulates mesangial cell proliferation and cell death, leading to glomerulosclerosis. Such as the aforementioned glomerular hemodynamic changes, and high filtration state can lead to glomerular focal segmental sclerosis, and proteinuria. In addition, glomerular lipid deposition is also a focal segmental sclerosis CAUSE. Monocyte-macrophage cells or glomerular mesangial cells engulfed the deposition of LDL, the formation of foam cells (foam cells) and foam cells play an important role in the development of atherosclerosis, so the more support for glomerular focal segmental sclerosis and atherosclerosis, there is a common pathogenesis. Minimal change disease or membranous nephropathy lipids than the disease is higher, but the glomerular foam cell infiltration are not severe and the disease.Glomerular fat calm can also cause glomerular capillary endothelial cell injury, as well as platelets, macrophages, monocytes, aggregation, stimulate the production of cytokines such as IL-1, of TGFβ, these make the mesangial cell proliferation, extracellular matrix components increased and the glomerular capillary lumen clotting.
(4) single-macrophages within the glomerular infiltration of mononuclear macrophages can produce a variety of cytokines, such substances to stimulate mesangial cell proliferation leading to glomerulosclerosis. Of the disease, monocyte-macrophage cells and histocompatibility antigens (MHC) of the number of positive 1a cells increased the number of these cells with focal segmental sclerosis lesions consistent. The cells and the cell adhesion molecule (ICAM) can activate macrophages, and glomerular macrophage activity. The same time, the monocyte-macrophage cells of the renal interstitial apparent infiltration, infiltration and proteinuria and renal function consistent with the extent of damage. In addition, the glomeruli of the above-mentioned lesions and cholesterol levels and obesity development process is also relevant. Interstitial mononuclear macrophage infiltration reduce the prednisone treatment, along with improved renal function, but glomerular cell infiltration and sclerosis is difficult to reduce the proteinuria will not improve.
Segmental glomerular capillary loop coagulation allows activation of the platelet release of platelet-activating factor (PAF), platelet-derived growth factor (PDGF), these factors effect caused in the mesangial lesions. Experiments show that the anticoagulant such as heparin, warfarin, or thromboxane inhibitors, can reduce the glomerular focal segmental sclerosis lesions, reduce proteinuria, without affecting renal blood flow and glomerular filtration rate.
Plasma factor effect of the disease after renal transplantation can rapidly recurrence, the recurrence rate of up to 35% ~ 50%. Therefore, considering that there may be some plasma factors cause the disease. Some people have in recent years immunoadsorption treatment for the patients and allows urine protein to reduce urinary protein complex l stop adsorption, re-adsorption can still make urine protein decreased, suggesting that the blood of patients with a glomerular capillary loop permeability The increase of material.
Visceral epithelial cell lesions occur in the disease development, not only the mesangial matrix plays an important role, and epithelial cells in lesions of the disease starting stove.Pathological observation noted that the onset of the disease both the visceral epithelial cell hypertrophy (hyperplasia), cytoplasm diluted with capillary loop mast, while the filtrate leakage of poor filtration area increases, the formation of false cells. With hypertrophy and dilatation of the capillary loop with fake cell adhesion in the glomerular capsule, forming the start of segmental sclerosis stove On this basis, the development of sclerosis.
Genetic factors compatriots, relatives of the disease report few, but there are all the same report of the disease in MHC antigen donor kidney transplant recurrence rate was 82% recurrence rate of 53%, not identical related kidney other allogeneic donor kidney recurrence rate of 35% is highly suggestive of genetic factors. In laboratory animals also has the obvious tendency of the germ line.

The incidence of chronic nephritis, which the law

Chronic nephritis is a kidney disease, people should be understood This is becausemany people will be unaware that they have on chronic nephritis, including some children.People, especially to have some knowledge of its etiology and pathogenesis, in normaldaily life to protect your body.
1, chronic nephritis may be acute nephritis evolved, and the situation is more common.The onset of acute glomerulonephritis, the failure to completely control the persistence ofclinical symptoms and urinary protein, persistent for more than a year, and become achronic nephritis. Past history of nephritis, significant symptoms of edema and massive proteinuria and nephrotic syndrome due to upper respiratory tract or other infections.Does have a history of acute nephritic syndrome, recuperating after a few weeks or months after the clinical symptoms and urinary abnormalities disappeared, normalkidney function. After a longer interval (the elderly up to years), upper respiratory tract or other infections or overwork, the sudden appearance of proteinuria, edema, or (and) high blood pressure, nephritis symptoms.
2, there are some patients in the past and not too chronic nephritis, but it will suddenlyshow corresponding symptoms. Past, no history of nephritis, short-term proteinuria, theheld hypertension and (or) renal insufficiency. The past, no history of nephritis, hematuria and proteinuria (or) due to infection or after exertion, to reduce or disappear soon aftershort-term rest. This recurrent, without obvious clinical symptoms.
Thus, the etiology of chronic nephritis of this nephropathy is more complex, and some patients from the development of diseases such as acute nephritis some patients thedisease due to past history of kidney disease, some patients are not related the historyof the disease, but will suddenly show corresponding symptoms have on chronicnephritis.

How to effectively curb the disease of chronic nephritis

In life, everyone should be aware of the chronic nephritis nephropathy characteristics ofthis, it's a long course, and during the onset of the disease is easy to deteriorate, to bringthe patient's health damage is self-evident. Therefore, for patients with chronic nephritis,the main treatment focus is to curb the progress of the disease, the following give you about two daily measures.
1, the proper exercise
Patients with chronic nephritis should not put an end to long-term exercise, the promotion of rehabilitation is extremely unfavorable. The doctors recommend that patients take the necessary exercise methods to adhere to in daily, so as to more effectively alleviate the condition. For patients with chronic nephritis, due mostly Qiyinliangxu after a long illness,the lack of righteousness, physical activity should be mainly a small amount of exercise, such as, jogging, walking, Qigong, and guide, tai chi, so that blood Nobumichi, bonesstrong and solid, but be careful not too tired.
2, there are often personal
Do this for patients with chronic nephritis is very necessary, can play a key nursed back to health role. Suffering from this disease, the patient should follow the seasonal changes, to be living there often, this is a useful measure of the good control of the disease. As early as the Qin period, found that adapt to climate change of the seasonsseason has an important impact on human health and disease, so people want tomaintain the normal physiological function of health and longevity, periodic changes inthe nature of yin and yang seasons made adaptive regulation, otherwise they will become students or lead to various diseases. Patients with kidney disease, pooradaptability, low resistance to disease, should conform to the four seasonscorresponding Heaven.
Daily chronic nephritis patients need to actively nursed back to their own constitution, andthis is very useful to promote the treatment of the disease. If the condition of chronicnephritis, malignant transformation, then the patient's health damage will increase,therefore, patients need to actively take measures to curb the progress of the disease.