Pressure Dacheng adolescents nephropathy incentives

As competition intensifies, young people facing increasingly heavy pressure of studies, and studies of many families in order to develop high-quality children, registration of a variety of training, specialty classes, to enable young people to the normal patterns of life are not a good match. Some young people all day indulging in online games such as abnormal regulation of life, the child's endocrine system disorders.
Nephropathy symptoms occult, coupled with the child described on autonomic symptoms is unclear, it is difficult to get the attention of parents. Once the obvious symptoms of the kidney has been severely compromised. Clinically often see this kind of situation: children swollen body, the parents realized their children had kidney disease, and then have missed the golden era of treatment, leading to disease protraction. Some parents are unable to choose a regular hospital and treatment, resulting in irreversible damage to the child's kidneys, is this the wrong choice and even cause the child had uremia.
The majority of adolescents and kidney disease can be cured, you must attach importance to the early detection of kidney damage signal "," urine screening is to find early renal damage signal "The easiest way to. Nephropathy no special clinical signs, and prevention of kidney disease to do the following:
First, regular medical examinations, especially in the beginning of the test and college entrance students before and after early examination and entrance examination must be done urine.
Second, we must grasp the basic knowledge of kidney disease, such as a urine test must be done in the waist and knees and knees, anemia, edema, hematuria, nausea, vomiting and other symptoms.
Third, should always carefully observe and ask the child if it is found the above symptoms, timely treatment.
Fourth, in the diagnosed children have kidney disease, be sure to go to a large kidney specialist hospital for treatment. Nephropathy is not a high incidence and clinical experience of the common species, the doctor has a decisive role for the treatment. Large kidney specialist hospital patients, the doctor's clinical experience, the treatment effect.

Nephropathy fewer bananas - and 60-year-old ate two bananas and nearly died

Elderly people suffering from kidney disease in order to promote the metabolic cycle, before going to bed eat two bananas. These two bananas almost to the life of the elderly: At midnight, the old man's heartbeat, blood pressure, breathing a sudden emergency. After investigation, the elderly suffering from acute hyperkalemia, if treatment is not timely will be life-threatening. The doctor pointed out that kidney patients are the best eating potassium-rich fruits, and bananas is such fruit!
Before going to bed two bananas old man nearly died
61-year-old Mr. Wong insists on hemodialysis has been more than two years, usually three meals a day care. The evening of the 17th before going to sleep, he felt a bit hungry, but also expect to go to the hospital the next day to do dialysis, can the body's metabolites are discharged, then ate two bananas. At 0:00 on the 18th, Mr. Wong suddenly twitching limbs, lying on the side of his wife woke up, the call of Mr. Wong but there is no response. She immediately dialed 120. A few minutes later the ambulance arrived, carrying Mr. Wong rushed to a nearby hospital.
"Fortunately, sent in a timely fashion, if the night will be life-threatening!" Director of renal medicine physician, patient breathing was weak, and lower blood pressure, high potassium and the heart rate is particularly low, only 19 beats / minute (normal is 60 per minute - 100 times). By oxygen after, recovery heart rate a series of rescue, the midway patient cardiac arrest, but in the end saved the day.
Two bananas almost lost his life? "The face of the families questioned, the doctor explained, normal eating potassium fruit is no problem, because in the process of urination, the body of potassium will be discharged. Renal failure or uremia patients, usually urinate is not a lot of metabolites in the body is not with the urination. High potassium fruits are bananas, watermelon, kiwi, etc., so patients with renal insufficiency, if you urinate less or even not urinate, do be careful not to eat the fruits of potassium is too high, try to eat other fruits.
In addition to bananas, kidney patients can not eat the fruit?
Nephrotic syndrome patients can not eat watermelon: watermelon water content, is the good fruit of the summer the summer heat, but the meat is cold, the elderly physically weak persons eat more prone to abdominal pain or diarrhea; heart failure and edema of the severity of the patient should not eat.
Nephrotic syndrome patients can not eat a Persimmon: Persimmon meat contains a lot of tannin, persimmon plastic phenol, tannin convergence and strong, so constipation patients should not eat. In addition, fasting eat persimmons or extend their fresh persimmon, easy diospyrobezoar. Therefore, gastritis, hyperacidity, spleen and stomach Deficiency patients, and fasting, tiredness best not eat or Eat a persimmon.
Patients with nephrotic syndrome can not taste lychees: the lychee continuous consumption, make people look pale, resulting in dizziness, palpitation, cold sweats, yawning, weakness and other symptoms, which is due to the lychee caused by exogenous low blood sugar reactions. medically known as "litchi disease".

How serious is the nephrotic syndrome?

How serious is the nephrotic syndrome?Many patients are very concerned about the treatment of nephrotic syndrome, the patients in order to a good understanding of nephrotic syndrome is necessary. So, nephrotic syndrome is serious, and made to explain to everyone, I hope we can help.
First we explain the disease complications of nephrotic syndrome
First, due to the large number of immunoglobulin is lost in urine, plasma protein reduced impact of antibody formation. Application of adrenal corticosteroids and cytotoxic compounds, in which patients body defenses are weakened and prone to infection, such as skin infections, primary peritonitis, respiratory tract infections, urinary tract infection, and even induce sepsis.
Second, patients with nephrotic syndrome often have hyperlipidemia, and hypercoagulable states, and therefore prone to coronary heart disease. Coronary heart disease has become a cause of death of nephrotic syndrome factors (after infection and renal failure).
Third, the complications of nephrotic syndrome What are prone to thrombosis in patients with nephrotic syndrome, especially Membranous glomerulonephritis the incidence of up to 25% to 40%.
Fourth, patients with nephrotic syndrome due to massive proteinuria, hypoalbuminemia, hyperlipidemia, often in the low blood volume and a hypercoagulable state in vivo, vomiting, diarrhea, use of antihypertensive drugs and diuretics diuretic can make a sudden decrease in renal blood perfusion, and thus reduce the glomerular filtration rate, leading to acute renal failure.
Disease complications of nephrotic syndrome, we all understand it, if you do not have good control of the disease, disease progression, this is likely to develop into uremia, so patients must be very good control of the disease.

IgA nephropathy patients diet what needs attention

Patients with IgA nephropathy diet what needs attention? Many kidney patients are very concerned about, understanding of patients in normal life, eating is not very comprehensive, and patients to a good understanding of the diet of the iga nephropathy, this is very helpful for the treatment of Experts to give you to make explanations, I hope we can help.
1, the supply of protein
IgA nephropathy in the diet should be based on the degree of impairment of renal function to determine the protein intake. Longer duration of renal damage is not severe cases, the protein in the food you do not have strictly limited, but should not exceed 1 gram per kilogram of body weight per day, high-quality protein to achieve 50% or more.
2, the supply of energy
Because some patients limits the protein, the heat supply to the carbohydrate and fat as the main source of energy supply, as the labor intensity. The rest, adult daily supply of 30 to 35 kcal / kg body weight. And to meet the needs of the patient's activities.
3, the control of sodium intake
Should be considered in patients with or without hypertension and edema were treated with salt, no salt diet. Severe edema and hypertension, the amount of sodium to control the less than 2 g / day, or even to give salt-free diet, is generally appropriate to the low-salt. Also fasting other salty food and sugar drinks and pungent foods.
4, limiting the intake of potassium
IgA in patients with oliguric (daily urine output of less than 1000 ml), then high potassium foods such as kelp, seaweed, animal offal, bananas, citrus, potatoes, tomatoes, squash, tea, soy sauce, MSG, etc. need to limit.
5, the intake of water
IgA nephropathy patients should drink plenty of water or drink. If there are no special circumstances, such as disease doctor told him to let more than to drink water and other, more important aspect of drinking water in IgA nephropathy diet care, family members can also urge patients to drink plenty of water. IgA nephropathy is the further development of renal insufficiency, uremia, in addition to strictly limit the protein, but also strictly limit the intake of water.
6, vitamin supplements
Any IgA patients in the daily diet should be given plenty of vitamins, especially vitamin C, because long-term IgA nephritis patients may have anemia, vitamin C can increase iron absorption and should supplement rich in vitamin B and folic acid food, to correct anemia.
Patients with IgA nephropathy diet what needs attention? We should be the diet of patients with IgA nephropathy need to pay attention to have a certain understanding. Experts suggest that patients should reasonably arrange their own diet, to promote the optimal therapeutic effect.

Long-term state of fatigue wary of chronic kidney disease strikes

The working pressure is too large, long-term work overtime to stay up all night and other factors, makes the modern city long-term state of fatigue. Research pointed out, the body long-term state of fatigue, alert to the emergence of chronic kidney disease.

Chronic kidney disease has become one of the world's epidemic diseases do not usually have obvious symptoms, nearly 80-90% of patients undiagnosed.
Tired for many reasons, Chenda Long said that the pressure and other psychological factors that may make people feel tired; sleep, infection, endocrine disorders and other physical problems can also cause fatigue. Therefore, unusual tiredness, unexplained chronic kidney disease should also pay attention to whether the
Deterioration of kidney disease progress is usually quite slow, chronic kidney disease is divided into five, early symptoms, the patient is easy to overlook, but to wait until symptoms appear, usually 4 to 5, it was too late. Therefore have to rely on urine tests, blood tests and ultrasound scans in order to early detection and early treatment.
Kidney disease patients in addition to regularly track renal function tests and other biochemical values​​, should also bear in mind that control of blood pressure, moderately reduce the protein intake.

Nephrotic syndrome in serious condition?

The nephrotic syndrome is now more common form of kidney disease, many patients and friends want to know the nephrotic syndrome serious? Nephrotic syndrome will lead to renal failure?
First of all, we explain what are the complications of the nephrotic syndrome
First of all, due to the large number of immunoglobulin is lost in the urine, plasma protein reduced the impact of antibody formation. Application of adrenal corticosteroids and cytotoxic compounds, in which patients body defenses are weakened and prone to infection, such as skin infections, primary peritonitis, respiratory tract infections, urinary tract infection, and even induce sepsis.
Second, patients with nephrotic syndrome often have hyperlipidemia, and hypercoagulable states, and therefore prone to coronary heart disease. Coronary heart disease has become a cause of death of nephrotic syndrome factors (after infection and renal failure).
Third, the complications of nephrotic syndrome What are prone to thrombosis in patients with nephrotic syndrome, especially membranous nephropathy, the incidence of up to 25% to 40%.
Fourth, patients with nephrotic syndrome due to massive proteinuria, hypoalbuminemia, hyperlipidemia, often in the low blood volume and a hypercoagulable state in vivo, vomiting, diarrhea, use of antihypertensive drugs and diuretics diuretic can make a sudden decrease in renal blood perfusion, and thus reduce the glomerular filtration rate, leading to acute renal failure.
How to complications in patients with timely and effective treatment, a long time will develop into renal failure, so patients must be early detection and early treatment.Disease control is very helpful.
Severe nephrotic syndrome? Through this introduction, we nephrotic syndrome should have a good understanding.

Chronic kidney disease is a lifestyle disease

Chronic kidney disease is a lifestyle disease
Many people diagnosed with chronic kidney disease, it felt like my world had ended.Western reporters from the combination of prevention and treatment of chronic kidney disease forum was informed that in the major cities in China, chronic kidney disease with a high incidence of every ten people in this disease. However, the development of early chronic kidney disease to end-stage renal failure, there is a very long time, patients can be regulated in a regular hospital kidney specialist treatment and lifestyle modifications, can delay the deterioration of renal function.
Ten patients with chronic nephritis
Professor Wang Tao, the In recent years, China Beijing, Guangzhou and other big cities of chronic kidney disease was 10%, and the incidence increases with age and increased the suffering of the population aged 60 -70 years old male disease rate as high as 23.8%, females 27%.
Studies have shown that the elderly, hypertension, diabetes, obesity, and repeated with a variety of drugs, family history of chronic kidney disease, such as population, belong to a high risk of chronic kidney disease. Chronic kidney disease early can not have any symptoms, even if symptoms are not typical, is often overlooked, delaying the timing of treatment. It can be said that chronic kidney disease is often overlooked "silent killer".
Patient is the protagonist, the doctor is the coach
Many people diagnosed with chronic kidney disease, it felt like my world had ended. In fact, studies show that fact, if the early intervention and treatment, control of risk factors can delay the progress of chronic kidney disease, and even reduce the incidence of renal failure.
Knows or suspects that he is in chronic kidney disease and the best regular kidney specialist treatment, and cause of screening and treatment programs, the establishment of. Chronic kidney disease is a chronic kidney damage (usually more than three months), collectively referred to by many diseases, disease treatment and prognosis is not exactly the same.
Professor Liu Xusheng chronic kidney disease patients to enter in the diagnosis after a long treatment period, if a local hospital for chronic disease management clinic is best transferred to the outpatient treatment. Different from the traditional acute disease, chronic kidney disease, its treatment goal is not to cure, but allow patients to resume a normal life. Drug treatment is not the core, the adjustment of the patient's lifestyle is the key to prevention and treatment of chronic kidney disease. Chronic disease management clinic doctors to establish health records for patients, time to guide patient referral review system to grasp the changes in the patient's condition, doctors and even arranged for the patient "homework", outpatient extended to the family. This mode of treatment, the patient is the protagonist, the doctor is the coach.
The two professors pointed out that although there are many drug treatment of chronic kidney disease, but studies show that chronic kidney disease is a lifestyle disease. The one hand, the disease caused by chronic kidney disease, and lifestyle are closely related to factors that play an increasingly important role which the renal damage caused by diabetes mellitus, hypertension-induced renal damage is the main reason for the occurrence of chronic kidney disease. As we all know, the occurrence and development of diabetes, high blood pressure is closely related and lifestyle. On the other hand, lifestyle factors is an important cause of kidney disease progression. Practice shows that patients with chronic kidney to control salt intake, increasing physical activity, smoking cessation and other lifestyle changes can effectively lower blood pressure, slow the progress of renal damage. Therefore, it is recommended that chronic kidney disease patients to pay attention to their daily diet, coupled with the medication, in order to play effectively.

Nephropathy in patients with eating misunderstanding

In kidney patients, eat and drink is very important, because of the need to import food by renal excretion, believe it will increase the burden on the kidneys. However, in life, many patients in the diet, mishandled, or chaos fill to eat, or the diet is too strict, that it makes the condition ups and downs. Kidney disease, experts say in the diet, kidney patients must pay attention to the low-salt, low fat, high-quality low-protein, light digestible best tonic must consider the physical condition before, under the guidance of a doctor, dialectical implementation.
Some patients said that my kidney problems can be much more to eat tonic. This is not the right extreme point of view. Many drugs are excreted from the kidneys, and therefore need to carefully measure the benefits of drugs and medication burden to the kidney.
Question 1
Patients with kidney disease can eat meat?
Under normal circumstances, eat into the body of the plant protein to metabolic changes, and finally most of the nitrogenous waste excreted by the kidneys. Therefore, eating too much protein-containing food, will increase the burden on the kidneys.
Kidney disease, experts say, is generally recommended that patients with nephropathy, protein intake is 0.6 grams per kilogram of body weight. For example, in patients weighing 60 kg, the intake of protein a day for 60 × 0.6 = 36 grams every two meat contains 9 grams of protein, so kidney patients day eat about two 4 meat.
Containing proteins in the food we eat daily, more or less, including meat, eggs, milk protein quality, high utilization of the human body, can be used to repair or maintain muscle strength, others such as beans (green beans, red beans etc.), stone fruits (peanuts, melon seeds, cashews, etc.), whole grains, sweet potatoes, taro, potato, vegetables, fruits contain protein quality is poor, will create more waste, kidney patients intake of protein to animal protein-based, and also to control the amount of 3-4 two-meat can be.
Question 2
Patients with kidney disease can not eat salt?
Folk often think that patients with kidney disease must quit the salt ", repeated the baseless assertion, mistakenly not shallow. We know that salt is an essential ingredient of the human body, long-term salt will lead to electrolyte imbalance, such as hyponatremia, the body adversely.
Kidney disease, experts say, matter what kind of nephritis, absolute quit salt is wrong. Should be considered when the patient has significant edema or increased blood pressure, reducing salt intake, so as not to aggravate the sodium retention. When the patient clinically and no edema or hypertension, salt intake does not have more restrictions.
Generally speaking, are suffering from kidney disease, oliguria, hypertension, edema either case should limit salt intake, mild edema and hypertension salt intake of 2-3 g / day; a high degree of edema to avoid salt, so the ring does not quit the salt depends on the disease situation.
Question 3
Kidney patients drink Diet soup?
The food is diverse, as long as renal function is normal, what to cook soup for strictly limited. Fish, chicken, lean meat, eggs, soup, add some herbs can also as the Diet. Such as Codonopsis, the Beiqi pot chicken, lotus, Mainz real burning lean spleen, cordyceps stewed duck Kidney Yin, soil Fuling to burn turtles can Yin and diuresis. Liu Xusheng renal insufficiency in patients with gout should be taken to avoid drinking the old fire soup, because soup purine on renal function, may induce gout.
In clinical practice, the experts found that some patients always thought that traditional Chinese medicine non-toxic, there are some herbs (such as Guan Mu Tong) may have serious kidney damage after taking the drug in cases of acute renal failure in nonvolatile memories.
In addition, the renal toxicity of traditional Chinese medicine cantharidin, centipede, bee venom, cinnabar, realgar, red lead, Motherwort, Magnolia, Asarum, Hook, Arrowhead Mountain, pornographic films, these drugs must be strictly followed in the use the range, and careful application.
Question 4
Kidney patients a day to drink plenty of water?
A healthy day for adults at least 1200 ml of water to drink. However, acute Chronic nephritis, acute renal failure, oliguria, and nephrotic syndrome, chronic renal failure with oliguria edema patients, to control the amount of drinking. Otherwise, go to drink did not break out, and water retention in the human body to increase the edema, but also easy to increased blood pressure, this time, the amount of water the day before urine output plus 500 ml is appropriate.
Kidney disease, experts say, usually one day's urine output was 1200-1500 ml when urine output is increased, the amount of water can be relaxed. In addition, the drinking water for dialysis patients, depending on the circumstances may be. Just the start of dialysis due to the presence of some residual renal function, a certain amount of urine, with the prolonged duration of dialysis, residual renal function is gradually lost, the urine output is less and less, the need for strict control of water intake.
There is a saying in the past: that dialysis patients can let go of the food and drink, the present point of view: peritoneal dialysis patients there are also excessive volume load, the patient can be expressed as edema, poor blood pressure control, the same should follow "Expenditure and Revenues" principle.

10 details of the defense nephropathy

A high incidence and high mortality of the disease, kidney disease, early symptoms are very subtle, and many people are often unwittingly suffering from kidney disease.
The kidney is a tube of "detoxification", it is healthy, it is not good, the plot Poison body. Everyone is clear the importance of protection of the kidneys, can be in daily life, injury to the kidney "has no intention to move, but everywhere, many people Shangqie do not know who the danger is approaching. What to pay attention to details?
Eat salty
Also likely to lead to high blood pressure. Hypertension is a systemic disease, kidney disease and it often is a pair of twin sisters. In recent years, the incidence of hypertension caused by kidney damage is on the rise. Therefore, in daily life should adhere to the salt diet, daily intake of salt should be more appropriate in the 5-6 g.
Eat large amounts of sugar, too much oil
Will not only increase the burden on the kidneys, but also lead to obesity. Obesity can cause kidney fat content increased, weight increased, the volume increases, glomerular hypertrophy. Obese patients are also prone to insulin resistance, triggering diabetes. About nearly 40% of diabetes patients with diabetic nephropathy, and this kidney disease is one of the most difficult to treat kidney disease.
Protein overeat
Will lead to elevated serum uric acid concentration of the body, causing hyperuricemia. Serum uric acid concentration increased toxicity to the kidney is very large and can easily lead to renal tubules and renal interstitial lesions occur, and finally develop into chronic renal failure, uremia.
Long-term use or large doses of anti-inflammatory analgesic drugs
Such as the painkiller tablets, indomethacin, acetaminophen, aspirin, etc., easily lead to kidney damage. Kidney damage can be expressed as: fatigue, dry mouth, loss of appetite, frequent urination, urgency, dysuria, or hematuria and sterile pyuria, and accompanied by joint pain and other symptoms. Some directly cause acute nephritis or glomerular necrosis, nephrotic syndrome, severe cases can cause kidney failure and death.
Overdose of some Chinese herbal medicine
In recent years, the clinical constantly found that taking certain Chinese herbal medicine (including medicine) can cause renal damage. Would "kidney injury" of Chinese herbal medicine: the Tripterygium manshuriensis, Pharbitis, Xanthium, poppy capsules Health Aconitum, so that a gentleman, green wood, wide Menispermaceae and so on. The Tripterygium lead to kidney damage, followed by manshuriensis. Manshuriensis kidney injury because containing aristolochic acid renal toxic substances.
Overeating
The modern dinner more opportunities, often eating too much delicious food intake will eventually produce waste - uric acid and urea nitrogen. These wastes are mostly excreted through the kidneys, excessive eating will undoubtedly increase the burden on the kidneys. Often holding back urine of some people busy for a long time holding back urine. Urine in the bladder for too long it is easy to the growth of bacteria, the bacteria will retrograde through the ureter to the kidney, leading to urinary tract infections and pyelonephritis. These infections, recurrent, can lead to chronic infection and difficult to cure. Patients will not only back pain, urinary urgency and other symptoms may develop into acute uremia.
Excessive drink
Excessive intake of soft drinks and sports drinks will be indirect damage kidney. The body's pH 7.2, these drinks are generally highly acidic body pH change significantly after drinking. The kidneys regulate the pH of the human body organs, long-term excessive intake of soft drinks and sports drinks, would burden the kidney to increase the probability of kidney damage.
Drink drink tea
Some people think that the drink to drink tea can sober up, in fact, this is not only ineffective, but also harm to the kidneys. Rapid theophylline in tea can affect the kidneys play a diuretic effect alcohol has not yet had time to re-decomposition begins with kidney discharges stimulate the kidney by a large number of ethanol, which damage the renal function.
Ignore the cold
A cold to eat antibiotics can damage the kidneys, if dragging is not a doctor, ignoring treatment does not seem severe cold, pharyngitis and other diseases may lead to kidney disease.
The study found that the incidence of acute glomerulonephritis, mostly associated with hemolytic streptococcus infection, and this the onset of nephritis have a certain incubation period, patients are generally cold symptoms were relieved or dissipated before the symptoms of nephritis. Mainly as follows: hematuria, the urine turbid reddish brown; edema, and most of them first appeared on the face, especially in the eyelid, there will be serious in the lower extremities, in addition, headache, nausea, vomiting, fatigue, weakness , loss of appetite and other systemic symptoms. Therefore, after the cold of the above symptoms, we must not neglect the treatment of acute nephritis.
In addition to common upper respiratory tract infection, pneumonia, hepatitis and other common infectious diseases will lead to different types of kidney disease. Ding Xiaoqiang Director recommends that the daily life in order to protect the health of the kidneys, should strengthen exercise, pay attention to rest and improve the body immunity, to prevent the colds, do not let the virus damage the kidneys.
Long-term holding back urine
Daily life in some obscure bad habits will lead to kidney disease. Therefore, even if the work is again busy, do not forget the ground to drink water and go to the toilet on time. Once you develop the habit of holding back urine, they will unwittingly affect the health of the kidneys. Kidney disease at an early stage is often no specific symptoms, many patients are in late stage when the acute attack or disease into regret.
In addition to regular urine and kidney function tests, can not be ignored in daily life, especially backache, edema, changes in urine color, increased nighttime urination, symptoms such as anemia or high blood pressure permanently. If they find traces of kidney disease, must be timely treatment.

FGS prognosis

Of FSGS and poor prognosis, 25% to 30% and 30% to 40% 5 years and 10 years into the renal failure. 10% to 20% of the pediatric the OK dialysis or renal transplant recipients caused by the disease. The following clinical and laboratory indicators for estimating the prognosis of a certain reference value: (1) Clinical manifestations: non-selective proteinuria may be invalid prednisone severe persistent proteinuria and manifested as nephrotic syndrome is often the H-resistant creatinine level, acute renal failure and poor prognosis. (2) morphological changes: the lesions in the urinary pole that is, state-of-the-art disease, better prognosis, and prognosis of lesions around the vascular pole or the mixed type, the collapse associated with poor outcome. Associated with the development of interstitial fibrosis to the possibility of chronic renal failure. (3) The other accompanied circumstances: racial genetic backgrounds (Africa and Spain, children with poor prognosis, poor prognosis of a positive family history), adult patients, the prognosis is less favorable than those children, human immunodeficiency virus infection and heroin, cocaine, a drug abuser with poor prognosis.

High rates of renal transplantation recurrence of FSGS is generally believed that 25% to 40% recurrence after transplantation, 20% to 50% within five years, once again lose their kidney function, a higher relapse rate in OK kidney transplant again up to 80%. Related kidney transplantation than cadaveric renal higher relapse rate. Recurrence of FSGS often to glucocorticoid resistance, although the report cyclophosphamide (8 to 12 weeks, 1 ~ 2mg * kg-1 * d-1) allows long-term remission [15]. Early plasma exchange could prevent FSGS recurrence remains to be documented.

FSGS diagnosis

(1) how to reduce the rate of misdiagnosis. FSGS is a morphological diagnosis of an organization, in view of the hardening of the small ball as a focal distribution, found only in early disease nearly medullary renal unit, it is easy to misdiagnosis. In recent years, scholars have stressed the need for a sufficient number of biopsy specimens, and stressed that found a segmental sclerosis of glomerular enough to be diagnosed as of FSGS. According to probability estimates, 10 glomerular specimens missing rate of 35%, 20 glomerular enable the missed rate dropped to 12%. Authors suggest that, if the credibility of the FSGS diagnosis 95%, 99%, 99.5%, the minimum number of glomerular consecutive imprints on each cross-section need be for 7,8,9, but the slice cross sectiondistance of less than 27μm or 23μm [8]. Material restrictions not found in the glomerular segmental sclerosis, following 3:00 prompt FSGS have a certain reference value, namely (1) abnormalities of glomerular hypertrophy. A pediatric small lesions that later develop into FSGS the glomeruli than their peers in the control group and re-biopsy is still minimal change glomerular increased significantly. (2) with minimal change in the foot process fusion completely compared to that of FSGS foot process fusion is incomplete. (3) of FSGS is often accompanied by varying degrees of renal tubular damage, so check to see the small tube of focal atrophy with interstitial change is also a valuable reference.
Two different parts of the glomerular sclerosis. In recent years, noted that FSGS sclerosis lesions have a different distribution in the glomerulus, and its primary disease due and prognosis. Common change of five kinds: (1) hardening occurs in the glomerular urinary pole. (2) glomerular sclerosis occurs in blood vessels with a very transparent degeneration. (3) glomerular sclerosis in the capillary loop margin with parietal epithelial cell adhesion. (4) collapse of glomerular sclerosis. (5), diabetic nephropathy unique to tuberous sclerosis and hyalinization of the capillary arteries. Due to the cause, the variety of pathophysiological mechanisms of glomerulosclerosis area can see Schiff acid-positive cell-free material, but its composition may be different. In the glomerular vascular pole most of the renal atrophy and poor prognosis; located in the urinary pole, the so-called cutting-edge lesions, suggesting that the early lesions, the prognosis is good. The margin of lesions are most common in the pediatric, mixed lesions and vascular pole lesions is more pronounced in adults, but all the hardened forms can be found in all age groups. The morphological characteristics of illness thus different. Secondary to reflux nephropathy, often around the renal capsule fibrosis and Bowman's capsule, interstitial thickening and spotty scarring. Heroin kidney epithelial cells change, the onset of interstitial fibrosis and tubule damage bit more obvious. The human immunodeficiency virus (HIV) infection caused by focal scarring, severe renal damage, including cystic dilatation, as well as glomerular vascular atrophy and electron microscopy to see the network organization gathered on the endothelial cells.
3. Except of systemic disease or primary renal disease secondary of FSGS. : Confirm the primary or idiopathic FSGS, except a variety of secondary glomerular hypertrophy / hyperfiltration due to of FSGS (such as solitary kidney, reflux nephropathy, unilateral renal resection, a variety of reduced nephron caused by kidney disease, diabetes, hypertension, obesity, sickle cell disease, etc.) and due to renal scarring cause of FSGS (such as IgA nephropathy, polyarteritis, lupus nephritis, hereditary nephropathy, etc.). In addition, the need to except the human immunodeficiency virus infection and heroin, cocaine addict kidney changes.
Commonly used clinical indicators in glomerular diseases FSGS diagnosis and its severity predicted value. Of FSGS clinical: 97% had proteinuria, microscopic hematuria 91%, hyperlipidemia 83%, 68% of the urinary tube, hypertension 67%, 50% of nephrotic syndrome, renal dysfunction, 47%, family history of 11 %.
Due to the trauma of the kidney biopsy, kidney disease scientist trying to explore some of the features associated with the indicators to be diagnosed and prognosis. (1) urinary protein often clues of FSGS, but neither diagnosis is difficult to estimate the extent of of FSGS. Proteinuria is mainly caused by the non-hardening of the permeability of the glomerular capillary wall abnormalities, no direct correlation with FSGS. And extensive glomerular sclerosis, proteinuria but started to decrease. Furthermore proteinuria and glomerular capillary hemodynamic abnormalities. Therefore, to improve the hemodynamic drugs such as angiotensin converting enzyme inhibitors, although in the short term to reduce urinary protein but does not affect the morphology. (2) serum creatinine is also commonly used clinical indicators, FSGS can uniquely affect the glomerular filtration function activated, and some lesions of glomerular function decreased by other alive glomerular function enhanced to compensate, so the FSGSdegree and creatinine levels can be very different. (3) changes in glomerular filtration rate (GFR): FSGS is usually accompanied by a small tube between the different levels of quality change, the lack of the integrity of the tubule, GFR markers, such as creatinine, can reflux back into the blood circulation, rather than from the urine, leading to underestimate the level of GFR. And renal blood flow change can also affect the GFR.Some antihypertensive drugs (angiotensin converting enzyme inhibitors), effectively reduce glomerular capillary pressure, which led to the decline in GFR. Such a drastic decline in GFR is not caused due to deterioration in FSGS organizations learn.
To sum up, this feature of FSGS - the reason for the discrepancy in the structure can be summarized as: (1) focal segmental distribution of lesions; (2) loss of renal units; (3) of the complete glomerular compensatory ; (4) renal blood flow change; (5) plasma osmotic pressure changes and changes in glomerular local pressure; (6) tubulointerstitial changes.

What are the cause leading to nephritis?

Nephritis is a major killer of human health, many nephritis patients want to understand the cause of the nephritis?
The present situation, has been considered hemolytic streptococcus infection is a major cause of the cause nephritis, recently found that infection of other pathogenic microorganisms and; the intrusion of some heterogeneous material, can cause nephritis.The cause of nephritis can be divided into the following categories:
Bacterial infection leading to glomerulonephritis: Streptococcus, Staphylococcus,pneumococcus, typhoid bacillus, diphtheria bacillus and M. leprae can be pathogenic;
Virus infection leading to chronic nephritis: including measles virus, varicella-zoster virus, hepatitis B virus; B virus, mumps virus, herpes zoster virus, and some tumor viruses and other infections;
Burgdorferi infection causes nephritis: such as Rickettsia, Treponema pallidum.
Parasitic infections leading to nephritis: such as trypanosomiasis, Luo Asi insects, Monteggia schistosomiasis, etc.;
Biological toxins invade the body leading to nephritis: such as pollen, bee venom;
Drug intoxication leading to nephritis: such as penicillamine;
Heavy metal poisoning leading to nephritis: such as gold, mercury, bismuth.
All these factors are the cause of nephritis, the above description, I believe you andnephritis have a certain understanding, if you want to know more knowledge about the cause of the nephritis

FSGS that continued progress may be

(1) growth factors. The basis put forward this doctrine: ① pathological mild hypertrophy with a small ball with mild sclerosis often coexist. FSGS glomerular volume significantly larger than the minimal change disease or normal controls. ② inhibition of specific growth factors can effectively prevent the development of glomerular sclerosis.For example, an inhibitor of angiotensin Ⅱ by inhibiting platelet-associated growth factors and the transfer of growth factor β treatment of FSGS.③ the clinical lead to poor glomerular proliferation of abnormal factors, including hypoxia, hypertension and renal volume reduction, such as more than a kidney nephrectomy and unilateral renal dysplasia, often accompanied by the hair of FSGS. Molecular biology research from animal models and human biopsy data prompt The glomerulosclerosis each process is controlled by a major and several minor growth factor such as platelet-associated growth factors like early play an important role in hardening transfer growth factor beta hardening severity.
(2) hypertension. Glomerular pressure may impair kidney function and structure. On the contrary, reducing stress can improve and prevent hardening. Some people think that the pressure increased, the increase in capillary diameter, resulting in increased vascular wall tension caused by hardening. However, in the case of diabetic nephropathy and reflux nephropathy, glomerular increases than capillary diameter increased, but the vessel length extension and branch increase in the number; In addition, high blood pressure does not often appear in front of the glomerular sclerosis, as well as the The researchers found that only resection in nephron glomerular volume was significantly increased before the development of hardening. Therefore, high filtration, high perfusion pressure may not glomerular volume increase, or hardening of the only condition.
(3) the role and influence of proteinuria of FSGS progress: Some scholars believe that proteinuria itself may promote glomerular mesangial and epithelial cells or tubulointerstitial renal tissue scarring. Secondly, proteinuria can be induced by the inflammatory mediators, such as macrophages and TGFβ increased, leading to glomerular interstitial scarring.
(4) high cholesterol may affect the progress of FSGS. Foam cells, fat phagocytes with FSGS is more common. Some scholars believe that in the case of proteinuria, the filtered neutral fat matrix aggregation a specific pathogenic role [5,6]. Small lesions of lipids is also very significant and do not necessarily have hardened, it prompts the hyperlipidemia is only the cofactors of the hardening process.

Of FSGS start the factors

Of FSGS initiation factors not yet elucidated, but most scholars believe that thelymphocyte abnormal activation, release of lymphocyte factor, resulting in abnormalglomerular permeability and sclerosing changes. But results in abnormal glomerular capillary wall permeability and promote hardening factor remains unclear. The reportwould permit the experimental animals the presence of proteinuria lymphocyte-derivedfactor in FSGS patients. Some scholars believe that this cycle can change vascularpermeability factor can cause glomerular epithelial cell foot process fusion, resulting infoot process and basement membrane separation, followed by the basement membranepermeability changes in endothelial protein deposition, vascular loop necrosis, vascular loop and balloon adhesion, typical glomerulosclerosis change to.
Oxide production may be another important pathogenic mechanism observed in animal models of proteinuria, Mn - superoxide dismutase have increased the level of gene transcription in rat renal artery perfusion oxide.
FSGS have different characteristics in different ethnic groups. African-American andSpanish children from FSGS to terminal renal speed faster than the Caucasian, and theratio of the number. Related kidney transplant relapse rate than cadaveric renaltransplantation more, suggesting that genetic background plays an important role of FSGS pathogenic, but the specific genetic markers have not yet been confirmed.

Drug target for treatment of nephrotic

The scientists found a kidney disease can lead to kidney failure and other reasons, this finding may be able to bring a drug target for the treatment of chronic kidney disease.Focal segmental glomerulosclerosis (referred to as FSGS) is characterized by lesions and hardening of the tiny blood vessels in the kidneys, resulting in protein penetrate into the urine. There are no effective method for the treatment of FSGS, and its incidence is also increasing. By studying a large family of hereditary FSGS, Michelle Winn, and colleagues in the coding of a found a mutation in the gene of calcium into the cell protein.This ion channel proteins called transient receptor potential cation channel 6 or TRPC6.Because ion channels are usually susceptible to the influence of drugs, so this work will TRPC6 as a drug target for the treatment of chronic kidney disease a possibility.Previous studies have revealed that interrupt cytoskeletal and structural proteins of FSGS development process works.
Duke University Medical Center researchers have discovered a gene related to the type of chronic kidney disease. This disease called FSGS (familial focal segmental glomerulosclerosis) can cause complete renal failure, and affects 20% of dialysis patients. This finding will promote more effective treatment of this disease.
By the genetic composition of the detection of more than one multigenerational family with important types of FSGS, the researchers found something called TRPC6 (Transient Cycle Receptor Potential Cation Channel 6), a mutant form of the gene associated with the disease. Moreover, the function of this gene and related genes previously found in FSGS, these findings reveal a novel mechanism of renal injury. Targeting this ion channel drugs may effectively alleviate or prevent the scarring of the kidney. These channels are embedded in the membrane pore-like protein, able to control calcium flow. This gene represents the first with FSGS related ion channels. Winn et al. These findings are published in the May 5 online edition of Science magazine.
In the United States of FSGS incidence rate increases every year, and drug treatment of this disease is very limited and are non-specific drugs. So many patients to rely on dialysis to prolong life. Of FSGS etiology remains unclear, but previous findings suggest that the three other genes related with FSGS or class of FSGS disease. Previously identified genes responsible for the formation of the support membrane structural proteins. In 1999, the Duke research group identified in a New Zealand family with FSGS-related genomic regions.
In the latest study, researchers screened 106 individuals in seven generations and 600 members of the family, this narrowed it down to an exact gene - TRPC6. In this family, all FSGS members carry a TRPC6 gene mutation. Further study of variants of this gene in cultured kidney cells, this mutation responsible for the regulation of angiotensin II channel activity, angiotensin II can promote the occurrence of hypertension and kidney damage.
Although there are reports that TRPC6 mutations found in other hereditary FSGS family, but the findings on the role of this channel in kidney function problems bubbling to the surface. This channel may also be a new target for treatment of kidney disease.

On basic research in FSGS progress include

A plasma induced nephropathy factor previous evidence that the glomerular permeability factor is one of the reasons leading to FSGS, but has not clarified its essence. Infusion to rats with FSGS patient plasma, or serum extracts of staphylococcal protein A column can cause proteinuria. The extract of thermal instability, protease-sensitive, molecular weight of about 30 to 50 kDa, Podocytes in vitro incubation in plasma of patients with nephrotic syndrome enable podocytes of nephrin, podocin in and CD2AP molecules from the membrane translocation to the cytoplasm. Another study showed that normal human plasma in the plasma of patients with this role can be fully eliminated. Some scholars believe that there are protective factors in normal human plasma of FSGS patients lack the factor disease. The plasma in the end the existence of of FSGS protection molecules or pathogenic factor has not been fully elucidated.
The pathogenic role of podocytes in FSGS pathogenesis of podocytes gradually become the focus, the number of podocytes reduction is the main mechanism leading to glomerular sclerosis. The current positioning the podocyte hole membrane-associated molecules include: ① NPHS1 gene, the gene mutation is a major cause of nephrotic syndrome, Finnish type (CNF), and is mainly composed of two mutations (Fin major and Fin minor) due to massive proteinuria in NPHS1 gene knockout mice, their encoding nephrin molecules are also involved in enough cell signal transduction, including activation of the MAPK signaling pathway; ② The NPHS2 gene encoding podocin molecules can interact with nephrin and CD2AP may have a connection function of the gene mutation can lead to autosomal recessive inheritance of FSGS; ③ carrying CD2AP and its, it is located within the podocyte adapter molecules combine with the intracellular domain of the CD2 molecule, and nephrin anchored in the cytoskeleton, carrying CD2AP and its gene knockout mice manifested as nephrotic syndrome and renal insufficiency; ④ The ACTN4, which encodes the alpha-Actinin-4 is a muscle dynamic protein filaments cross-linked protein, is an important part of foot processes, to the maintenance of the skeleton of podocytes complete very important, ACTN4 gene mutations can cause autosomal dominant inheritance of FSGS, the ACTN4 knockout mice exhibit proteinuria and renal insufficiency; ⑤ The TRPC6, it encodes a calcium ion flow channel, TRPC6 gene mutations result in autosomal dominant genetic of FSGS.Found multiple mutations have contributed to the increase in calcium influx may therefore TRPC6 gene mutation as a functional (gain of function) pathogenic; ⑥ The PLCE1 gene, the gene mutation can lead to diffuse mesangial hyperplasia and FSGS lesions, thegene knockout zebrafish nephrotic syndrome.

Of FSGS treatment Introduction

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 of traditional Chinese medicine treatment of FSGS with 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.

New discovery of the new of familial FSGS susceptibility gene INF2 pathogenic mechanism

Recently, the international Biological Sciences Research top academic journals, "the U.S. National Academy of Sciences (PNAS), published online the latest achievements of the Shanghai Jiaotong University Affiliated Shanghai Children's Medical Center researchers. The new familial FSGS susceptibility gene the INF2 pathogenic mechanism for the new discovery "published article, the author is a child center pediatric into the Institute of Medicine, Department of Nephrology, the children's genetic disease task force member Dr. Sun Hua.
FSGS is a class performance for children and adults with kidney disease, chronic progressive glomerular diseases, the vast majority of clinical manifestations in patients with steroid resistant nephrotic syndrome. FSGS also contributed to the deterioration of renal function and chronic renal failure, the most important glomerular disease type, treatment antagonism exists, therefore, its pathogenesis and treatment strategies become hot and difficult in the field of diagnosis and treatment of kidney disease. The Shanghai Children's Medical Center is transformed into the Institute of Medicine Dr. Sun Hua group the use of cloning and mutation, as well as a series of protein interactions, the implementation of the pedigree linkage analysis was first discovered in the glomerular podocytes, INF2 negative adjustment of Rho / mDia was activated through interaction with the cell actin cytoskeleton regulatory protein mDia, cytoskeleton caused by heterogeneous and phenotypic changes of podocytes, thereby maintaining the normal function of podocytes, and confirmed that the INF2 pathogenic mutations interfere with this interactions lead to podocyte injury signal susceptibility, but also confirmed the new FSGS susceptibility gene INF2 mutations cause familial nephropathy. On this basis, the group further explore the pathogenic significance of these mutations, of FSGS susceptibility gene mutation is to affect or determine the clinical phenotype, disease progression, treatment response and prognosis, as well as important genetic factor for transplant relapse rate . The study comes from clinical cases of genetic data, from the molecular level interpretation of the INF2 mutations lead to the pathogenesis of FSGS, as well as the relationship of different mutations and different clinical phenotypes and prognosis. The study is also a very useful exploration of translational medicine and the practice of individualized treatment.
This research project has been the EPT of Shanghai Children's Medical Center of the Training Scheme funding; at the same time, Harvard Medical School hereditary kidney disease laboratory for this research project has also given strong support.

Hematuria of specific hazards?

Hematuria of specific hazards? A lot of people inadvertently found that his urine was brown or red, some people terrified to think she had any serious disease; some people because of no sense or hematuria come and gone and did not mind. Which Mody, what constitutes hematuria? Hematuria from where? What are the the hematuria hazards specific? Hospital experts to address these issues, as follows:
Urine routine examination, red blood cells per high power field over 3 medicine called hematuria. If the naked eye, hematuria, red blood or blood clots, called gross hematuria.To hematuria standard, but invisible to the naked eye, known as microscopic hematuria.Therefore, the hematuria is not the naked eye can judge, which is why do urine routine examination of one of the reasons. According to the accompanying symptoms, hematuria hematuria of pain and painless hematuria. Painless hematuria hematuria than the pain should arouse people's attention, because it is often an early signal of the urinary system tumors. Not urine red hematuria, sometimes to beware of counterfeit, such as the pseudo-hematuria, coloring urine, hemoglobinuria.
The potential danger of hematuria
Many people had hematuria no time to diagnosis and treatment, an important reason why these people hematuria did not feel any discomfort. As the saying goes, the dog bite is not called. Similarly, the most dangerous hematuria often is the kind of will not let you feel the pain, hematuria.
Special attention should be painless hematuria In addition to hematuria, it often have no other symptoms and discomfort and this hematuria without treatment may be temporarily disappear. Hematuria was intermittent, sometimes no. Every time after the disappearance of the hematuria, the patient always thought that the "disease" is also eliminated. In fact, this intermittent, painless hematuria, is often a clinical manifestation of tumors of the urinary system. Hematuria, a sudden increase, often late tumor. According to statistics, in patients with painless hematuria, bladder cancer accounts for almost 50 percent, accounted for 40% of renal cell carcinoma. Type of tumor mostly occurs in older people over the age of 40. Therefore, middle-aged, painless hematuria, we must remain highly vigilant. Hematuria began for the first time, you should identify the reasons for, do not delay.
Hematuria of specific hazards? Listened to the explanation of hospital experts, I believe we have learned about it, here, experts suggest that the majority of patients with a friend, to treat the disease must be timely diagnosis and timely treatment can not be blind to the effect, so as not to delay treatment, so that condition deterioration to patients with more serious injuries.

Progress in primary focal segmental glomerular sclerosis treatment

Focal segmental glomerulosclerosis (FSGS) is a group of similar pathological changes of chronic progressive glomerular disease, the characteristic pathological changes were part of the glomerular (focal, <50%, nearly marrow The glomerular easily sclerosis-like changes (matrix increase, capillary loop collapse) involved), part of the vascular loops (segmental vessels and vascular loops Yi involvement). FSGS was first described in 1957 by Rich in 1970 as an independent type of renal pathology. In recent years, renal biopsy data show that FSGS showed a trend of increasing year by year, and minimal change disease (MCD), mesangial proliferative glomerulonephritis (MsPGN) and FSGS can be transformed into each other. FSGS treatment response to glucocorticoids and cytotoxic drugs vary, their prognosis is directly related to the response to treatment, poor response to treatment are prone to chronic progressive renal damage, until the end stage renal disease (ESRD). The impact of FSGS is an important prognostic factor is the degree of proteinuria of FSGS's treatment objectives are: to reduce or eliminate proteinuria, prevent complications, slow down FSGS progress to ESRD. Are mainly elaborated primary FSGS treatment progress. 1 of FSGS glucocorticoid treatment.
The primary FSGS clinical performance as nephrotic syndrome, the majority reported that FSGS is not sensitive to hormone treatment, the response rate of eight weeks of the regular enough amount of hormone treatment of FSGS urinary protein less than 50% (average 20%). In recent years that, to extend the time of hormone therapy, may have more than 50% of FSGS in remission, glucocorticoid is still the first choice of FSGS treatment.
1 1 conventional method prednisone 1 5 2 0 mg / (kg • d), once every 4 to 8 weeks and achieved complete remission or partial remission (hormone-sensitive or sensitive part), prednisone can be gradually reduced the amount of maintenance treatment to more than 1 a or 1 a; sufficient quantities of prednisone treatment for four to eight weeks without remission (steroid-resistant), the joint use of immunosuppressive agents. 2 long course of hormone therapy program (1) Mendoza, program [4]: ​​① methylprednisolone intravenous pulse dose of 30 mg / (kg) (single maximum dose of 000mg): 1 - 2 weeks, every other day 1, 3 times / week; 3 - 10 weeks, 1 time / week; 11 - 18 weeks, every two weeks; 19 - 52 weeks, 1 times / month; 53 - 78 weeks, every 2 months to 1 year. ② prednisone oral dose of 2 mg / (kg) (single maximum dose of 60 mg): 1 - 2 weeks not 3 - 8 weeks, every other day, Dayton clothing, after the discretion to gradually decrease. The total course of treatment of men's-doza program, 5 a, the response rate and prognosis of urinary protein significantly improved compared with conventional hormone therapy program. (2) other long course of hormone therapy programs: the International Pediatric Nephrology Study Group (ISKDC) conventional treatment options recommended by the nephrotic syndrome did not distinguish between types of renal pathology, either MCD or of FSGS herein are prednisone 60 mg / (m * 2 d), in divided doses four weeks, followed by prednisone 40 mg / m 2, the next day orally for 4 weeks, tapering; the first 8 weeks of treatment of urinary protein-free remission are considered for steroid-resistant. Domestic pediatric prednisone 1 5 2 0 mg / (kg • d) After 8 weeks of treatment, remission, steroid-resistant criteria. However, the above criteria to judge the FSGS hormone resistance is not appropriate, and often lead to physicians reluctant to use hormone therapy, rather than FSGS real steroid-resistant, because the simple extension of hormone treatment can significantly improve urinary protein ease and prognosis. Experience in the treatment of adult FSGS: 8 weeks courses of sufficient quantities of hormones, sufficient quantities of hormone-induced FSGS urine protein remission time of 3 to 4 months of oral prednisone over 6 invalid before considering FSGS steroid-resistant.
But the lack of a long course of sufficient quantities of hormone treatment of FSGS samples and randomized controlled studies (RCT) data, its advantages and disadvantages to be subject to further evaluation, sufficient quantities of a long course of hormone therapy on children with adverse reactions (such as infection, growth developmental disorders, osteoporosis, high blood pressure and electrolyte imbalance, etc.), especially long-term effects can not be ignored.
2 combination therapy of FSGS
Of steroid resistance, dependence, frequency of recurrence of refractory primary of FSGS, in combination with other drugs to treat clinical inevitable choice.
2.1 cyclophosphamide (CTX) hormone the joint CTX treatment of FSGS common report, the CTX past as first-line drugs for the treatment of steroid-resistant FSGS. Rennert, etc. to the hormone oral and CTX intravenous pulse (at a dose of 500 mg / m * 2, the impact of 1 times / month) 6 months of treatment, results showed that 10 cases of steroid-resistant FSGS children, seven cases of complete remission, 1 cases partial remission (overall response rate 80%), two cases of no response. And CTX, Hari, etc. using the impact of hormone intravenous, oral treatment of 12 weeks, which, methylprednisolone 30 mg / kg or dexamethasone 5 mg / kg, every other day, six times every two weeks, four times, followed by a times / month, eight times, re-poured nylon oral tapering, were treated for 52 weeks. 59 cases of steroid-resistant FSGS patients with urinary protein / inosine values ​​from 10 0 to 0.75, serum albumin level rise by 19 g / L to 24 g / L; Among them, 17 cases of complete remission, eight cases of partial remission ; follow-up time of 3 of more than 34 cases, 22 cases (64.7%) with good prognosis, the majority of continuous complete remission. Gulati and so a prospective study: 1 / CTX shock, a dose of 500 to 750 mg / m * 2, while I poured nylon, four weeks before a dose of 60 mg / (m * 2 • d), then every other day taking splashed nylon (40 mg / m * 2) 4 weeks, decreasing the amount of 4 weeks is disabled. 20 cases of steroid-resistant FSGS patients, 13 cases of complete remission (65%), urine protein was negative CTX treatment time (12 ± 11.9) months follow-up time (21 2 ± 13 4) monthly urine protein continued negative. Bajpai and other every other day oral poured nylon and CTX intravenous pulse treatment of 24 cases of steroid-resistant FSGS patients, the CTX dose of 750 mg / m * 2, the impact of 1/6 months, only to find 7 cases of short-term (29. 2%) complete or partial remission, long-term follow-up only 5 cases (20.8%) remission, 17 cases of invalid (70.8%), and ease the untreated sensitive secondary steroid-resistant patients, suggesting that CTX on the original limited efficacy of drug resistance FSGS. Al Salloum et al reported 15 cases of steroid-resistant FSGS patients prednisone and CTX intravenous pulse therapy and were followed up for 4 years, prednisone 60 mg / (m * 2 • d) - 4 weeks, followed by every other day 40 mg / m * 2, 4 weeks, decreasing the amount of four weeks withdrawal; the CTX dose of 500 mg / m * 2, 1 / shock, 6 months. Were followed up for 4 years, 5 cases of primary resistant cases of treatment response (3 cases the development of chronic renal insufficiency), 10 cases of secondary resistance in patients with CTX pulse therapy is effective, but in the end are hormone-dependent, suggesting that hormone and CTX therapy for steroid-resistant FSGS, there is no significant effect, many studies also support the above conclusion.
Date, although some data show the efficacy of hormone and CTX treatment of drug-resistant FSGS, but still lack the RCT study, is generally believed that the subsequent secondary resistance in addition to the early governance hormone-sensitive FSGS patients have a certain effect, steroid and CTX treatment the efficacy of drug-resistant FSGS, there is no sufficient evidence. In addition, CTX adverse reactions (such as height, severe infections, hair loss, leukopenia, hemorrhagic cystitis, transient hypertension and drug injection, transient nausea, vomiting, etc.) must be given.
2.2 cyclosporine (CsA) of CsA is currently the treatment of FSGS have the exact effect of drugs, but usually require a longer course of treatment to maintain remission after renal toxic effects and withdrawal to recur is worthy of clinical attention. Mah-moud such as retrospective analysis of 106 cases to CsA treatment in patients with primary FSGS (45 cases of steroid-resistant, 61 cases of hormone dependent, of which 54 cases had received CTX treatment) of CsA starting dose of 6 mg / (kg • d), and gradually adjust the dose of CsA blood concentration maintained at 80 to 150 μg / L, treatment for 6 to 8 months after discontinuation of follow-up (6 ± 1 1 9) a. The rate of complete remission, partial remission rate and inefficiency were 71 7%, 7.5% and 20.8%. 31 cases but was discontinued in 91 cases of hormone relapse; 20 cases tried to stop the proteinuria disappeared CsA 16 cases immediately recurrence, and four cases, re-enable the CsA resistance. The results suggest that the significant effect of CsA on primary FSGS, but a higher relapse rate after stopping. Goumenos and other follow-up observation 5a CsA treatment, the efficacy of primary FSGS, with similar results. Recurrence of FSGS, Raafat large dose CsA treatment at a dose of 6 ~ 25 mg / (kg • d) of CsA by the low dose and gradually increase to remission or adverse renal effects until remission, CsA gradually reduction to the normal range, the results show a significant effect and can maintain for a long time in remission.
Long-term use of CsA adverse events (renal insufficiency, hypertension, gingival hyperplasia, hirsutism psychosis) is worthy of clinical concern. Chishti of a single small dose of CsA treatment of FSGS, the CsA dose (6 ± 0 8) mg / (kg • d), 1 / d, treatment time was 2 to 27 months without monitoring blood drug mass concentration. Results The total effective rate was 76% (16/21 cases), of which 52% (11/21 cases) in complete remission, partial remission 24% (5/21 cases), the onset time (2 ± 0 8 8 ) months; decreasing the amount of nine cases of complete remission of CsA withdrawal, including three cases of maintenance of remission (follow-up of 6 to 13 months), six cases of recurrence (follow-up 1.5 to 18. 7 months), recurrence of retreatment CsA or increased dose of CsA to sensitive. Treatment and follow-up period, CsA adverse reactions is small, suggesting that small-dose CsA treatment of FSGS is safe and effective. El - Husseini, 117 cases of children with primary FSGS to long-range small-dose CsA maintenance therapy of CsA starting dose is 5 mg / (kg • d), and gradually adjust the mass concentration of 1 to 2 months before the dose so that blood CsA Valley maintained at 100 ~ 150μg / L, after CsA plasma mass concentration maintained at 50 and with 100 μg / L, as long as proteinuria continue to ease of CsA blood concentration was maintained at 30 μg / L can also be low-dose CsA treatment time is 2 a (average 34 months), the results show a long time small dose CsA treatment of FSGS effective.
That CsA effectively reduce urinary protein and protection of renal function, used alone, especially with the hormone combination of CsA markedly hormone-sensitive FSGS, steroid-resistant and steroid-dependent children with primary FSGS have a certain effect. CsA as a steroid-dependent or steroid-resistant FSGS priority treatment options. CsA treatment should be emphasized that the individual differences of CsA dose can not be static, must adjust the dose according to blood concentration. It should be noted is easy to relapse after CsA withdrawal, and therefore adequate treatment, based on monitoring of adverse drug reactions (if necessary, repeat renal biopsy for renal tubulointerstitial injury), maintenance treatment is required more than 1 a.
2.3 other immunosuppressants new immunosuppressive agents try for the treatment of drug-resistant FSGS, including mycophenolate mofetil (MMF), he tacrolimus (FK506) and Manila neomycin, reported a lot, but Case, the efficacy of different, but its low toxicity and a more significant effect demonstrated its good prospects and look forward to the findings of the RCT. Joint and sequential use of immunosuppressive therapy for refractory of FSGS, is expected to achieve better results. Type of renal pathology, such as el - Reshaid, reported 21 cases of steroid-resistant MCD or FSGS patients with nephrotic syndrome treatment: the initial application of 12 weeks of CsA or of FK506, and then 3 months of MMF, and then 3 months MMF plus of CsA; if not complete remission in the MMF plus CsA on the basis of 1 / impact of CTX, three times in a row; complete remission plus complete remission after 3 times with 1 / CTX impact, every four months, decreasing the amount of MMF or CsA to the minimum dose to maintain urine protein negative; such as the above-mentioned program has not yet reached complete remission, repeated 1 time / month impact of CTX three times, plus methylprednisolone pulse therapy for 3 consecutive days. changed to oral prednisone and tapered. Immunosuppressants used in conjunction with the experience is not yet mature, but has a different mechanism of action combined with different immunosuppressive agents, and thus a synergistic therapeutic effect, will reduce the amount of immunosuppressants, and reducing the adverse effects of immunosuppressants advantage.
2.4 other ancillary drugs such as angiotensin-conversion enzyme inhibitors (ACEI) and (or) the use of angiotensin II receptor antagonist (ARB), as well as for high cholesterol lowering therapy, for a hypercoagulable state anti- coagulation therapy, have helped to reduce proteinuria and slow the deterioration of renal function and FSGS progress to ESRD can be used as adjuvant therapy for high blood pressure and antihypertensive treatment.
3 FSGS non-drug treatment Replacement of low-density lipoprotein (LDL), immunoadsorption and plasmapheresis can be used as adjuvant therapy for the treatment of refractory FSGS. In view of hyperlipidemia, especially high LDL effects on the kidneys, reported LDL replacement can make proteinuria reduced to improve the response rate and delaying the progress of renal pathology. Plasma replacement therapy can be used for the treatment of recurrent FSGS after kidney transplantation, plasma exchange before kidney transplantation, urine protein to reduce migration to maintain graft function have a certain effect; but the mechanism of humoral factors in FSGS is not yet clear. the efficacy of plasma exchange still need to be further determined.